DISORDERS 

OF  THE 

HEART  BEAT. 

THOMAS  LEWIS. 


SECOND  EDITION 


UNIVERSITY  OF  CALIFORNIA 
AT  LOS  ANGELES 


GIFT  OF   CAPT.  AND   MRS.- 
PAUL  MCBRIDE  PERIGORD 


UNIVERSITY  of  CALIFORNIA 

AT 

LOS  ANGELES 

LIBRARY 


Digitized  by  the  Internet  Archive 

in  2007  with  funding  from 

Microsoft  Corporation 


http://www.archive.org/details/clinicaldisorderOOIewiiala 


CLINICAL  DISORDERS 


OF    THE 


HEART    BEAT 


A    HANDBOOK    FOR    PRACTITIONERS    AND 
STUDENTS. 


BY 


THOMAS   LEWIS,  M.D.,  D.Sc,  F.R.C.P., 

Assistant  Physician  and  Lecturer  in   Cardiac  Pathology,  University  College 
Hospital,  Physician  to  Out-Patients,  City  of  London  Hospital 
,    ■  for  Diseases  of  the   Chest. 


LONDON  :  .  NEW  YORK  : 

SHAW  &  SONS,  PAUL  B.  HOEBER, 

FETTER  LANE,  E.C.  69  EAST  59TH  STREET. 


1914. 

136524 


L58  < 


PREFACE  TO  FIRST  EDITION. 


THERE  can  be  but  few,  engaged  in  the  active 
practice  of  medicine,  who  are  not  aware  that 
a  new  and  important  chapter  has  been  added 
to  our  knowledge  of  the  mechanism  of  the 
heart  beat  during  recent  years.  The  newly- acquired 
information  has  been  gathered  by  the  employment 
of  precise  graphic  methods.  Those  who  are  engaged 
in  studying  the  heart  and  its  defects  by  means  of 
o>    special  instruments,  are  fully  conscious  of  the  burden 

C<1 

OS 

^  which  awaits  the  student  or  practitioner  who  has  yet 

o  to   bring    himself   abreast   the   times   in  this  field  of 

<d  knowledge. 

g  A  question  is  often  put  to  some  of  us.     In  what 

^  degree  is  an  acquaintanceship  with  the  new  methods 

-g  essential  or  expedient  in  the  routine  of  busy  practice  ? 

08 

O 


iv.  Preface. 

The  graphic  study  of  heart  affections  is  but  one  of 
many  clinical  and  pathological  subjects  which  has 
forged  ahead  of  late  years.  While  a  medical  man 
can  ill  afford  to  neglect  the  advance  of  a  subject  in 
which  he  practises,  he  may  act,  in  a  too  vigorous 
pursuit  of  one  branch  of  medical  science,  to  the 
detriment  of  his  knowledge  in  other  directions.  A 
universal  and  detailed  acquaintanceship  with  medical 


science  as  it  .exists  to-day  is  no  longer  possible,  but 
it  behoves  all  practitioners  to  grasp  new  principles 
and  to  be  aware  of  their  influence  upon  the  care  of 
patients  afflicted  with  common  maladies. 

If  I  am  asked  whether  it  is  essential  that  a  prac- 
titioner of  general  medicine  should  be  trained  to  record 
the  movements  of  the  several  heart  chambers,  I  am 
inclined  to  reply  that  the  acquisition  of  the  special 
manipulative  skill  and  the  necessary  experience,  which 
the  obtaining  and  accurate  interpretation  of  graphic 
records  involves,  entails  too  great  an  expenditure 
of  time  and  energy  adequately  to  repay  him  or  the 
patients  he  serves.  And  my  reply  is  dictated  by 
the   belief   that   most   of   those   disturbances   of   the 


Preface.  v. 

heart's  mechanism  which  are  met  with  in  everyday 
practice  can  be  identified  by  simpler  means. 

Reflections  of  this  kind  influence  me  in  offering 
to  medical  men  a  small  handbook,  which  I  trust  may 
inform  them  of  the  new  facts  and  conclusions  which 
are  of  chief  service  at  the  bedside. 

I  have  confined  the  reproduction  of  graphic  records 
almost  to  such  as  illustrate  what  may  be  seen  and 
felt,  for  many  disorders  of  the  heart  can  be  identified 
by  sight  and  touch  when  these  senses  are  aided  by 
hearing.  A  single  and  portable  piece  of  apparatus 
may  be  used  in  cases  of  doubt  and  difficulty,  to  supple- 
ment the  observations  so  obtained.  The  Dudgeon 
sphygmograph  is  probably  familiar  to  most  medical 
men  ;  fitted  with  elastic  bands  of  attachment,  and 
preferably  with  a  time-marker  also*,  it  readily  allows 
a  short  strip  of  radial  pulse  curve  to  be  obtained. 
Such  a  curve,  alone,  will  usually  place  the  observer 
in  possession  of  facts,  which  are  sufficient  for  an 
analvsis   of   the   common   disturbances   of   the   heart 


*  The  complete  apparatus  is  supplied  by  S.  Shaw,  Esq.,  of  Padiham, 
Lancashire,  at  a  moderate  cost. 


vi.  Preface. 

beat.  The  use  of  the  sphygmograph  encourages 
accuracy  ;  yet,  as  I  hope  to  show,  a  great  deal  can 
be  accomplished  without  it. 

In  the  succeeding  chapters,  I  have  not  attempted 
to  acquaint  the  reader  with  the  evidence*  upon  which 
the  diagnosis  of  the  several  cardiac  disorders  rests, 
but  have  recounted  such  physical  signs  as  I  have 
found  serviceable  in  identifying  these  disorders, 
prior  to  the  application  of  more  precise  methods 
in  individual  instances. 

To  ascertain  the  nature  of  the  heart's  mechanism 
in  a  given  patient  is,  as  we  shall  see,  of  twofold  value. 
It  is  of  importance  in  elucidating  the  remaining 
physical  signs,  especially  those  of  auscultation  ;  and  it 
seriously  affects  the  attitude  towards  the  patient,  for 
it  often  influences  the  prognosis  and  treatment  pro- 
foundly. The  recognition  of  the  existing  mechanism 
is,  as  experience  has  so  often  shown,  one  of  the  very 
first  essentials  in  the  care  of  cardiac  cases. 


*  A  full  account  of  such  evidence  may  be  found  by  those  who  desire 
it  in  my  recent  publication,  "  'J  he  Mechanism  of  the  Heart  Beat,"  published 
by  Messrs.  Shaw  and  Sons,  London. 


Preface.  vii. 

Such  new  facts  as  may  be  found  in  the  chapters, 
have  been  collected  largely  during  the  tenure  of  a  Beit 
Memorial  Fellowship,  to  the  Trustees  of  which  it  is 
my  desire  to  state  this  obligation.  That  the  reader 
may  benefit  from  a  fuller  experience,  I  have  not 
hesitated  to  take  advantage  of  the  published  works 
of  other  writers  on  the  same  subjects.  It  is  pleasurable" 
to  acknowledge  the  kindness  of  my  friend  and  colleague 
Dr.  T.  R.  Elliott,  for  his  criticism  of  the  chapters 
and  for  his  careful  perusal  of  the  proof  sheets  ;  and  I 
am  grateful  to  all  my  colleagues  at  University  College 
Hospital  for  the  generous  manner  in  which  they 
have  placed  their  material  at  my  disposal. 

Th.  Lewis. 
Decevnber,  1911. 


(     viii     ) 


PREFACE  TO  SECOND   EDITION. 


The  speecty  exhaustion  of  the  first  edition  of  this 
handbook  preserves  it  for  the  most  part  in  its  original 
form.  A  richer  experience  has  confirmed  my  belief  in 
its  conclusions. 

The  chief  alteration  is  the  addition  of  a  short 
chapter  upon  Auricular  Flutter,  a  condition  which  has 
come  to  light  but  recently.  Special  opportunities  of 
studying  this  curious  disorder  enable  me  to  sketch 
its  chief  features. 

27,   Queen  Anne  Street, 
August,  1913. 


(     ix     ) 


CONTENTS 


CHAPTER     I. 

The    recognition    and    identification  of     disorders    of    the 
cardiac  mechanism 

Preliminary  evidences 

Age  and  frequency  ;  heart  rate  ;  persistence  of  irregularity. 

Common  types  of  disorder  and  their  meaning 

Solitary  pulse  intermittences ;  coupled  beats ;  triple 
beating;  halved  pulse  rate;  a  grossly  irregular  pulse; 
a  mild  grade  of  irregularity. 


Page. 


CHAPTER  II. 

Sinus  irregularities 
Definition 

The  nature  of  sinus  disturbances 
Respiratory  irregularities 

Sinus  irregularities  which  bear  no  relation  to  respiration 
The  recognition  of  sinus  irregularities 
The  prognostic  significance  of  sinus  irregularities 


8 
8 
8 
11 
14 
14 
15 


x.  Contents. 

CHAPTER  III. 

Heart-block        . .  . .  . .  . .  . .  . .  . .  . .  16 

Definition  .  .  . .  .  .  . .  .  .  . .  .  .  . .  16 

The  nature  of  heart-block  .  .  .  .  .  .  .  .  . .  16 

Etiological  and  pathological  relations    .  .  .  .  . .  .  .  20 

Age  ;  sex  ;  heredity  ;  relations  to  infective  diseases  ; 
relation  to  chronic  degenerative  processes  of  more  obscure 
origin  ;  heart-block  as  a  result  of  digitalis  administration  ; 
morbid  anatomy. 

The  recognition  of  heart-block     .  .  .  .  . .  . .  24 

Effects  on  the  circulation  and  the  general  symptomatology  .  .  31 

The  prognosis        . .  .  .  .  .  .  .  .  .  . .  . .  34 

The  treatment         . .  .  .  .  .  .  .  . .  .  .  .  .  36 

CHAPTER  IV. 

Premature  contractions             . .          . .          . .  . .  . .  . .  39 

Definition  . .          .  .          .  .          .  .          . .  .  .  .  .  . .  39 

The  nature  of  premature  contractions    .  .  . .  .  .  .  .  39 

Etiological  and  pathological  relations    .  .  .  .  .  .  .  .  42 

Age  ;    sex  ;    associated  conditions  and  provocative  factors. 

The  recognition  of  premature  contractions        .  .  .  .  .  .  45 

The      subjective     phenomena    which    accompany    premature 

contractions     .  .  .  .  .  .  .  .  .  .  •  •  •  •  51 

The  prognosis  and  treatment       .  .  .  ■  .  ■  •  •  •  •  52 


Contents. 


XI. 


CHAPTER  V. 

Simple  paroxysmal  tachycardia 

Definition 

The  nature  of  simple  paroxysmal  tachycardia 

Etiological  and  pathological  relations 

Age ;  sex ;  heredity  ;  relations  to  infective  disease  ; 
associated  conditions  ;  factors  promoting  attacks  ;  morbid 
anatomy. 

The  recognition  of  simple  paroxysmal  tachycardia 

Symptomatology  of  paroxysmal  tachycardia 

Differential  diagnosis 

The  prognosis 

The  treatment 


55 
55 
55 
57 


59 
62 
64 
66 

68 


CHAPTER  VI. 

Auricular  flutter            . .          . .          . .          . .  .  .  .  .  . .         71 

Definition  .  .          .  .          .  .          .  .          .  .  .  .  .  .  .  .          71 

The  nature  of  flutter        .  .          .  .          .  .  .  .  .  .  .  .          71 

Etiological  and  pathological  relations     .  .  .  .  .  .  . .          74 

Age ;   sex  ;    relations  to  infective  disease,  etc.  ;    associated 
conditions ;  morbid  anatomy. 

The  recognition  of  flutter             .  .          .  .  .  .  .  .  . .          74 

During  the   2  :  1  heart-block  phase  ;  during  the  stage  of 

irregular    responses  ;    when  the  responses  of  the  ventricle 
are  infrequent. 

The  symptomatology  of  flutter     .  .          .  .  .  .  .  .  ■ .          77 

The  prognosis        .  .          .  .          .  .          .  .  .  .  •  •  ■  •          80 

The  treatment        ..          .,          ..          ..  ..  ..  ..          81 


Xll. 


Contents. 


CHAPTER  VII. 

Auricular  fibrillation   .  .          . .          . .          . .  . .  . .  . .  82 

Definition  .  .          .  .          .  .          .  .          .  .  .  .  .  .  .  .  82 

The  nature  of  auricular  fibrillation      .  .  .  .  .  .  .  .  82 

Etiological  and  pathological  relations     .  .  .  .  .  .  .  .  84 

Age  ;    sex  ;    relation  to  infections,  associated  conditions  ; 
morbid  anatomy. 

The  recognition  of  auricular  fibrillation  . .  .  .  . .  87 

The  general  symptomatology        .  .          .  .  .  .  .  .  .  .  92 

Remarks  upon  diagnosis              .  .          .  .  .  .  .  .  .  .  95 

The  prognosis        . .          . .          .  .          . .  .  .  . .  . .  96 

The  treatment         .  .          .  .          .  .          . .  .  .  .  .  .  .  97 

Paroxysmal  fibrillation     .  .          .  .          . .  .  .  .  .  .  .  101 


CHAPTER  VIII. 

Alternation  of  the  pulse         . .  . .  . .  . .  . .  . .  103 

Definition  .  .  .  .  . .  .  .  . .  .  .  .  .  .  .  103 

The  mechanism  in  alternation  of  the  pulse  .  .  . .  .  .  103 

Etiological  and  pathological  relations    .  .  .  .  . .  .  .  104 

The  recognition  of  pulsus  alternans      .  .  .  .  .  .  . .  105 

The  subjective  sensations  of  patients  presenting  pulsus  alternans  107 

The  prognosis        .  .  .  .  .  .  .  .  . .  . .  .  .  108 

The  treatment         .  .  .  .  .  .  .  .  .  .  .  .  .  .  ]09 

Index  . .  .  .  .  .  , .  .  .  ,  .  , .  ,  .  ,  .  \\q 


Chapter  I 


THE     RECOGNITION     AND     IDENTIFICATION     OF 
DISORDERS    OF   THE   CARDIAC   MECHANISM. 

It  seems  desirable  that  I  should  open  the  chapters  of 
this  book  by  acquainting  my  readers  with  the  general 
arrangement  of  the  matter  contained  in  it. 

Since  those  who  work  amongst  the  sick  usually  discover 
a  real  interest  in  a  particular  phenomenon  by  observing  it 
rather  than  by  reading  of  it,  I  begin  the  first  chapter  with  a 
general  description  of  the  chief  derangements  of  the  rate  and 
sequence  of  the  pulse  and  heart  beat  as  they  are  felt,  seen, 
or  heard  by  all  practitioners.  I  take  certain  common  and 
generally  recognised  physical  signs  as  they  are  noted  at  the 
bedside  and  translate  these  signs  into  terms  of  mechanism, 
without  attempting  to  describe  the  manner  in  which  they  are 
brought  about  and  without  suggesting  their  value  in  prognosis 
or  treatment.  I  shall  speak  of  sevejoiorms  of  cardiac  disorder, 
and  they  will  be  described  under  theJY>11  owing  headings  : — 

1.  Sinus  arrhythmia. 

2.  Heart-block. 

3.  Premature  contractions. 

4.  Simple  paroxysmal  tachycardia. 

5.  Auricular  flutter. 

6.  Auricular  fibrillation. 

7.  Alternation  of  the  pulse. 

There  may  be  some  to  whom  these  terms  are  still  un- 
familiar  or   to   whom   their   meaning   is   still   obscure.     My 


Chapter  I. 


immediate  endeavour,  therefore,  is  to  offer  them  a  preliminary 
idea  of  the  meaning  of  these  names,  an  idea  which  I  hope 
may  appeal  to  them  from  their  past  experience  ;  and  I  do 
so  by  citing  clear  examples  of  phenomena  to  which  in  future 
I  must  perforce  refer  by  the  use  of  distinctive  names. 

If  we  feel  the  pulse  of  a  young  adult,  when  his  inspiration 
is  deep,  or,  better  still,  if  we  feel  the  beating  of  a  dog's  heart 
against  its  chest  wall,  a  periodic  jrregularity  of  the  pulsa- 
tions is  observed  which  follows  the  sejDajate  acts -of  .breathing. 
"T^cite  this  disorder  of~the  heart  beat  as  a  characteristic 
example  of  sinus  arrhythmia,  or  one  in  which  the  whole 
heart  is  involved. 

a  In  many  patients  in  whom  the  radial  pulsations  and  heart 
beats  run  with  perfect  uniformity  for  long  periods,  an 
occasional  and  isolated  disturbance  is  noticed.  The  -pulse 
intermits  ;  it  loses  one  of  its 


its  at  interva1g-~-When . 


the  heart'  is  examined  it  is  found  that  at  Jth^mqmentjaf  the 
disturbance  a  ventricular  contraction  appears  before  the- 
rhythmic  beat  is  due,  and  that  this  early  beat  is  followed  by 
a  pause  of  unusual  length.  I  cite  this  disturbance  as  a  simple 
example  of  ^what  I  shall  in  future  describe  as  a  premature 
-contraction,  and  what  has  usually  been  referred  to  in  the  past 
as  an  "  extrasystole." 

"s"  If  in  a  similar  case,  where  the  ^c^asionjj^jrulse  fails, 
a  similar  failure  of  ventricular  action  is  jiiscQveTech-so--that 
on  hstemngjit  the  apjg^Ffeeatlno  abnormal  ^sounds  are  heard, 
but  the  heart  remains  silent  throughout  the  whole  of  the 
pause,  th^^henomena^axe„-eAdolences_jof  anotheiL_condition , 

n^mej^heartJilcck. But  lest  I  should  create  confusion  at  an 

early  stage,  I  must  add  to  this  example  the  statement  that 
heart-block  manifests  itself  in  many  other  ways  and  in  no 
way  which  stands  in  more  open  contrast  to  the  example  now 
cited  than  by  its  production  of  regular  pulses  of  conspicuously 
slow  rate. 


Disorders  of  the  Cardiac  Mechanism.  3 

Paroxysmal  tachycardia  is  a  term  which  is  probably 
familiar  to  all,  but  I  employ  it  in  a  restricted  sense,  and 
speak  only  of  instances  in  which  an_  absoluteJy__abrapt 
acceleration  of  regular  heart  beat,  which  subsequently 
terminates  in  an  equally  abrupt  manner,  is  repeated  from 
time  to, lime- 

From  time  to  time' we  find,  more  especially  in  the  elderly, 
regular  and  accelerated  heart  action  at  rates  of  120  to  160 
per  minute.  This  acceleration  is  notable  for  its  uniform 
rate  under  all  sorts  of  conditions  and  for  its  tendency  to 
persist  without  apparent  cause.  It  is  generally  the  result  of 
/  /  a  r  ic  ular^Jkiiizr . 

When  a  patient,  who  is  known  to  have  mitral  stenosis 
and  who  requires  treatment  for  cardiac  failure,  exhibits  not 
only  dropsy,  venous  engorgement  and  cyanosis,  but  a  rapid 
and  utterly  disordered  heart  action  in  which  there  is  no 
rhythmic  sequence,  he  presents  the  characteristic  picture 
~of  auricular  fibrillation. 

Finally,  if  in  a  case  of  renal  disease  or  arterio-sclerosis, 
thejpjilsc  tonsion  is  high,,  Cheyne-Stokes'  breathing  perhaps 
is  present,  and  the  pulse  is  regular  in  rhythm,  but  varies  in 
jorce  so  that  each  alternate  beat  is  strong  and  each  alternate 
beat  is  relatively  weak,  an  example jjf  alternation  glthe  pulse 
is  under  o^bs^ryation, 

I  have  deliberately  chosen  these  examples  because  they 
are  distinctive  ;  but  the  several  forms  of  disturbance  are  not 
.always  so  clearly  differentiated.  Were  it  so,  my  task  would 
be  simple.  The  examples  are  distinctive  and  consequently 
allow  a  preliminary  idea  of  the  meaning  of  my  terms  to  be 
entertained.  It  is  into  these  terms  that  I  shall  in  the  first 
instance  translate  the  commoner  physical  signs,  and  I  do  so 
with  the  object  of  providing  the  student  or  practitioner  with 
an  immediate  clue  to  the  type  of  mechanism  with  which  he 
is    dealing.     But    as    the    preliminary    description    will    be 


4  Chapter  I. 

inadequate,  it  is  supplemented  by  a  detailed  discussion  of 
each  form  of  disorder  in  the  remaining  chapters  of  the  book, 
in  which  an  account'of  the  pathology,  prognosis  and  manage- 
ment will  be  found. 
_  Preliminary  evidences. 

Age  and  frequency.  The  first  guides  to  the  identification 
of  a  disordered  heart  mechanism  are  the  age  of  the  patient 
in  whom  it  occurs  and  a  knowledge  of  the  frequency  of 
irregularities  at  different  ages. 

An  irregularity  of  heart  or  pulse  found  before  the  tenth 
year  is  almost  always  a  sinus  arrhythmia.  Heart-block 
may  be  present  during  the  first  decade  but  it  is  rare  ; 
a  few  premature  contractions  have  been  noted  in  quite 
young  children,  in  most  of  whom  extensive  enlargement  of 
the  heart  has  been  present,  or  during  the  course  of  acute 
infections.  Solitary  examples  of  auricular  fibrillation  have 
been  recorded  at  the  ages  of  5  and  13  ;  it  is  very  rare  before 
the  age  of  17. 

The    relative    frequency    of    disorders    of    the    cardiac 
mechanism  from  adolescence  to  old  age  is  in  general  hospital 
practice  approximately  as  follows  : — 

Auricular  fibrillation    .  .  .  .  . .  40% 

Premature  contractions  . .  . .         35% 

Paroxysmal  tachycardia,  sinus  arrhyth- 
mia, heart-block,  flutter  and 
alternation,  together  ..  ..  15% 

Dealing  with  those  in  whom  there  is  obvious  evidence 
of  cardiac  failure,  at  least  60%  of  irregular  hearts  are  irregular 
because  the  auricles  are  fibrillating. 

Heart  rate.  The  second  clue  is  the  rate  of  the  heart 
beat.  When  the  ventricle  beats  regularly  and  its  rate  is 
continually  below  35  beats  per  minute,  complete  heart-block 
(see  Chapter  III)  is  probably  present  ;  under  similar  cir- 
cumstances a  rate  which  lies  between  40  and  50  should  arouse 


Disorders  of  the  Cardiac  Mechanism.  5 

a  suspicion  of  partial  heart-block  ;  a  persistent  rate  of  130 
and  over  should  always  bring  to  mind  the  possibility  that  a 
long  continued  paroxysm  of  tachycardia  or  auricular  flutter 
is  present. 

If,  on  the  other  hand,  the  ventricle*  beats  irregularly, 
and  its  rate  surpasses  120  per  minute,  fibrillation  of  the 
auricle  is  probably  present,  and  as  the  rate  is  faster,  so  the 
probability  that  such  is  the  mechanism  approaches  certainty. 
Irregular  hearts,  beating  at  140  and  over,  are  scarcely  ever 
affected  in  any  other  manner.  Premature  contractions  very 
rarely  accompany  ventricular  rates  of  120  and  over  ;  sinus 
arrhythmias  are  almost  confined  to  rates  below  100  ;  and 
both  these  forms  of  irregularity  become  more  frequent  as 
the  scale  of  rate  is  descended  to  the  sixties  and  fifties.  If 
an  irregularity  is  observed,  and  the  rate  of  heart  beat  is  in 
the  neighbourhood  of  100,  any  influences,  such  as  exercise 
fever  or  the  administration  of  belladonna,  which  enhance 
the  ventricular  rate,  tend  to  abolish  all  irregularities,  with 
the  exception  of  that  due  to  auricular  fibrillation,  and  in 
this  instance  the  disorder  persists  and  is  often  augmented. 

Persistence  of  irregularity.  Auricular  fibrillation  is  usually 
a  persistent  condition  and  examination  from  hour  to  hour 
or  from  day  to  day  reveals  its  continual  presence.  The 
other  irregularities  are  usually  transient,  the  pulse  being  found 
to  be  quite  regular  from  time  to  time  ;  shorter  or  longer 
periods  of  normal  heart  action  intervene  between  periods  of 
disturbance. 

Common  types  of  disorder  and  their  meaning. 

Solitary  pulse  intermittences.  An  occasional  pause  of 
pronounced  length,  which  interrupts  an  otherwise  perfectly 

*  I   draw   especially   attention   to   the   distinction   between   ventricular 
irregularity  and  pulse  irregularity  ;   they  do  not  always  run  hand  in  hand. 


6  Chapter   I. 

regular  pulse,  is  due  to  one  of  two  causes,*  namely,  a  pre- 
mature contraction  (common),  or  a  dropped  beat  as  a  result 
of  heart-block  (rare).  They  are  easily  distinguished  ;  the 
premature  beat  is  felt  or  heard  at  the  apex  ;  it  gives  rise  to  an 
early  first,  or  first  and  second  sound.  In  block,  the  heart 
is  silent  and  motionless  during  the  whole  pause. 

Coupled  beats.  If  the  ventricular  beats  are  coupled  and 
the  couples  are  evenly  spacedf  they  are  the  result  of  one  of 
two  mechanisms,  for  either  the  alternate  beats  of  the  normal 
rhythm  have  been  replaced  by  premature  contractions — 
in  which  case  the  second  beat  of  the  couple  is  weak  and  may 
not  reach  the  wrist — or  else  each  third  ventricular  contraction 
has  been  lost  and  heart-block  is  present.  If  the  pulse  beats 
are  coupled  (pulsus  bigeminus)  a  third  possibility  remains  ; 
the  pulse  pairing  may  be  due  to  the  occurrence  of  premature 
heart  beats  which  replace  each  third  rhythmic  beat.  If  such 
is  the  case  the  premature  beat  will  be  appreciable  at  the 
apex,  though  it  does  not  reach  the  wrist. 

Triple  beating.  The  recognition  of  the  cause  proceeds 
along  similar  lines.  Tripling  at  the  apex  is  due  to  premature 
contractions  which  replace  each  third  rhythmic  beat,  or 
to  heart-block  in  which  each  fourth  ventricular  contraction 
has  been  lost.  Tripling  at  the  pulse  (pulsus  trigeminus)  may 
be  due  to  a  third  cause,  namely,  premature  beats  replacing  each 
fourth  rhythmic  beat,  the  early  beat  failing  to  reach  the  wrist. 

Halved  pidse  rate.  When  the  ventricle  beats  at  twice 
the  pulse  rate,  the  disorder  is  due  to  premature  contractions 
in  all  but  the  rarest  instances.     Alternation  has  been  known 

*  A  long  expiratory  pause  of  a  respiratory  arrhythmia  may  be  mistaken 
for  intermittence  if  the  examination  is  cursory. 

f  Sometimes  the  pauses  following  the  pairs  are  not  of  uniform  length. 
The  irregularity  is  then  a  complex  one  ;  it  is  due  to  auricular  fibrillation,  to 
which  premature  beats  have  been  added.  When  it  occurs  the  patient  is 
usuallv  under  the  influence  of  excessive  doses  of  digitalis. 


Disorders  of  the  Cardiac  Mechanism.  7 

to  occasion  halving,  the  weak  alternate  beats  failing  to  reach 
the  wrist  ;  but  this  condition  is  of  great  rarity  and  so  far  as  I 
know  is  only  very  transient.  The  two  are  readily  differentiated, 
for  in  the  first  instance  the  ventricular  beats  are  coupled 
while  in  the  last  they  appear  regularly. 

When  sudden  and  exact  halving  of  pulse  rate  is  noted  and 
the  ventricular  rate  is  halved  simultaneously,  the  disorder  is 
the  result  of  heart-block. 

A  grossly  irregular  pulse  in  which  there  is  hopeless 
jumbling  of  stronger  pulsations  with  quick  runs  of  almost 
imperceptible  beats,  and  in  which  the  lengths  of  intervening 
pauses  are  constantly  varying,  is  due  to  auricular  fibrillation. 

A  mild  grade  of  irregularity  which  persists,  which  is  not 
related  to  respiration  even  when  the  breathing  is  deepened 
and  in  which  no  definite  sequence  of  events  can  be  determined, 
is  also  due  to  auricular  fibrillation  in  most  cases.  A  similar 
irregularity,  which  shows  relations  to  respiration,  is  a  sinus 
arrhythmia. 

In  the  preceding  paragraphs  the  method  of  procedure 
at  the  bedside  is  briefly  stated,  and  an  acquaintance  with  the 
few  rules  which  I  have  given  will  enable  the  practitioner  to 
identify  a  very  large  number  of  the  disorderly  forms  of 
heart  action  with  which  he  meets.  But  where  the  reader  is 
in  doubt,  or  when  he  requires  more  explicit  information, 
in  regard  to  either  the  arrangements  of  the  beats  or  the 
manner  of  their  production,  or  in  respect  of  the  management 
of  the  case  in  which  the  disorder  is  discovered,  he  may  refer 
to  the  more  detailed  descriptions  contained  in  the  remaining 
chapters. 


(     8     ) 


Chapter  IT. 


SINUS    IRREGULARITIES. 


Definition. 


Irregularities  of  the  heart  which  are  produced  by 
interferences  with  the  rhythmic  impulses  at  the  seat  of  their 
discharge. 

The  nature  of  sinus  disturbances. 

In  a  discussion  of  sinus  irregularities,  the  nerve  supply 
of  the  heart  in  relation  to  disturbances  of  rhythm  occupies  a 
prominent  position.  Let  me  state  emphatically  at  the  outset 
that  we  have  nothing  to  do,  first,  with  the  functions  of  the 
intrinsic  cardiac  ganglia,  nor  secondly  with  the  sympathetic 
nerve  trunks  ;  as  we  have  little  or  no  real  knowledge  of  the 
part  they  play  in  disease,  so  any  theory  which  ascribes  a 
derangement  of  the  heart  to  a  perversion  of  their  functions 
is  without  practical  significance.  We  have  a  limited  but 
real  knowledge  of  the  vagus  and  its  relation  to  pathology  ; 
my  remarks  upon  the  cardiac  nerves  are  consequently 
confined  to  it. 

The  complete  beat  of  the  normal  heart  consists  of  a 
contraction  of  its  chambers  in  an  orderly  sequence.  The 
wave  of  contraction  starts  in  a  small  and  newly  discovered 
mass  of  tissue,  the  sino-auricular  node  (Fig.  1),  which  lies 
embedded  in  the  upper  and  anterior  end  of  the  sulcus  termin- 
alis.     The  sulcus  terminalis  runs,   as  may  be  remembered, 


Sinus  arrhythmia. 


9 


from  the  junction  of  the  right  auricular  appendix  and  the 
superior  vena  cava  towards  the  inferior  vena  cava  (see  Fig.  1). 
The  tissue  of  the  node,  consisting  of  a  specialised  network  of 
muscle  cells,  richly  supplied  by  the  nerves  of  the  heart  which 
enter  in  this  region,  lies  therefore  at  the  mouth  of  the  superior 


Sup  Vena  Cava 


51N0-AURICULAR 

Node 


Sulcus  Terminalis. 

.Auriculo  Vent  Bundle 
Left  Branch 

Foramen  Ovale 

.auriculo-ve-nt. 
Node 

Coronary  Sin  us 
Tricuspid  Valve 


Inl Vena  Cava 


Aorta 


RT  Appendix 


Fig.  1.  A  diagram  of  a  human  heart  (modified  from  Koch's).  The  walls 
of  inferior  vena  cava,  right  auricle  and  right  ventricle  have  been  partially 
removed  to  expose  the  septa.  The  position  of  the  sino-auricular  node, 
in  which  the  heart  beat  commences,  is  shown,  as  are  also  the  position  of 
the  auriculo-ventricular  node  and  the  course  of  the  auriculo -ventricular 
trunk  and  its  branches.  The  last-named  structures  convey  the  con- 
traction wave  from  auricle  to  ventricle. 

vena  cava  and  is  embedded  in  the  right  auricle.  The  con- 
traction which  commences  in  its  neighbourhood  spreads 
through  the  walls  of  both  auricles  and  is  transmitted  by  a 
special  band  of  tissue,  which  will  receive  subsequent  descrip- 
tion, to  the  ventricles.  The  orderly  rhythm  of  the  whole  heart 
takes  its  origin  in  this  node,  to  which  I  have  consequently 


10  Chapter  II. 

applied  the  term  heart's  "  pacemaker."  In  the  normally  acting 
adult  heart,  the  pacemaker  sends  forth  waves  of  contraction 
at  rates  which  average  72  per  minute,  and,  the  separate  beats 
being  evenly  spaced,  the  systoles  follow  each  other  in  a  regular 
order  or  rhythm.  The  pacemaker  is  under  the  control  of  the 
vagi,  or  inhibitory  nerves  of  the  heart,  and  they  normally 
exert  a  considerable  restraining  influence  upon  this  stimulus 
producing  centre.  Destruction  of  the  nerves,  more  especially 
that  of  the  right  side,  or  the  administration  of  atropine, 
which  paralyses  the  nerve  endings  in  the  heart,  raises  the 
rate  at  which  the  heart  beats  follow  each  other.  In  the 
human  subject,  the  probable  limit  to  which  the  rate  may 
rise  as  a  result  of  this  denervation  is  150-160  per  minute. 

In  many  subjects,  and  under  special  conditions,  the 
vagus  acts  with  excessive  inhibition,  either  persistently, 
or  rhythmically.  Its  influence  consequently  results  either 
in  a  uniform  pulse  slowing  or  in  a  waxing  and  waning  of  heart 
rate.  Let  us  deal  with  uniform  slowing  first,  for  it  is  a 
subject  with  which  we  are  only  briefly  concerned  in  these 
lectures.  Pronounced  slowing  of  the  whole  heart  is  com- 
paratively rare  ;  the  lesser  grades  of  slowing,  most  of  which 
are  probably  of  vagal  origin,  slowing  to  50  or  60  beats  per 
minute,  are  not  uncommon  and  are  especially  prominent  in 
athletes  and  in  association  with  increased  arterial  pressure, 
pregnancy,  jaundice,  aortic  stenosis,  convalescence  from  the 
acute  fevers  and  less  frequently  with  other  conditions.  Pulse 
slowing  of  this  degree  has  no  great  significance,  and  it  is  not 
uncommon  to  meet  with  people  who  enjoy  perfect  health 
and  in  whom  the  pulse  rate  lies  habitually  between  these  limits. 

Periodic  or  varying  disturbances,  which  influence  the 
rhythm  of  the  heart  at  its  source  and  produce  a  greater  or 
lesser  degree  of  arrhythmia,  are  of  greater  importance, 
though  it  will  only  be  necessary  to  describe  the  commoner 
forms  of  such  irregularities. 


Sinus  arrhythmia.  1 1 

In  Fig.  2,  a  diagram  of  a  characteristic  sinus  arrhythmia 
is  given.  I  shall  refer  to  similarly  constructed  diagrams  in 
succeeding  chapters.  The  figure  is  arranged  so  that  each 
narrow  black  rectangle  (^4)  represents  a  single  co-ordinate 
beat  of  the  auricle,  and  so  that  each  broad  black  rectangle  (V) 
represents  a  co-ordinate  ventricular  contraction.  Where 
an  auricular  contraction  is  followed  by  a  ventricular  response, 


I 


I 


Fig.  2.  A  diagrammatic  representation  of  the  action  of  a  heart,  affected 
by  sinus  arrhythmia.  The  contractions  of  auricle  and  ventricle  are 
represented  by  the  thin  and  broader  black  rectangles,  A  and  V  respec- 
tively. The  auricle  contracts  at  the  beginning  of  each  cycle,  and  sends 
its  impulse,  indicated  by  an  oblique  line,  to  the  ventricle,  which  responds. 
The  irregularity  consists  of  a  waxing  and  waning  of  rate,  in  which  both 
auricle  and  ventricle  participate. 

an  oblique  line  is  drawn,  joining  the  corresponding  rectangles. 
The  slope  of  the  oblique  line  indicates  the  time  interval 
between  the  contractions  of  auricle  and  ventricle.  All  such 
diagrams  read  from  left  to  right.  In  the  present  example,  a 
sinus  irregularity,  the  whole  heart  is  affected,  so  that  each 
ventricular  contraction  is  preceded  by  an  auricular  systole  at 
the  usual  interval.  The  irregularity  consists  of  a  gradual 
waxing  and  waning  of  auricular  rate  which  is  repeated 
periodically,  and  which  is  followed  exactly  by  the  ventricle. 

Res yiratory  irregularities . 

It  is  well  known  that  young  adults  manifest  a  very 
appreciable  irregularity  of  the  heart  and  pulse  rhythms 
when  they  breathe  deeply  (Fig.  3).  The  pulse  quickens 
while  the  chest  is  expanded,  and  slows  when  the  chest  is 
emptied.     But  in  both  young  adults  and  old  there  is  no 


12 


Chapter  II. 


respiratory  variation  of  pulse  rate,  which  the  finger  can 
discover,  while  the  breathing  is  natural.  On  the  contrary,  a 
perceptible  degree  of  natural  respiratory  irregularity  of  the 
pulse,  characterised  chiefly  by  one  or  more  long  pauses  during 
the  expiratory  period  (Fig.  4  and  5),  is  not  uncommon  in 
young  children,  and  sometimes  it  is  sufficiently  prominent  to 


Fig.  3.  A  sphygmographic  curve  from  a  normal  subject,  breathing  deeply. 
There  is  an  increase  of  pulse  rate  during  inspiration  and  a  decrease  during 
expiration. 


mm  rvwmm rmn  i  n>  i  WWWWWH  ■»>»»>■'  ■»■<»»> mutnrimn 


^M> 


■  •■•■I    ■  < 


Fig.  6.  A  gross  sinus  arrhythmia  ;  a  long  pulse  pause  accompanies  each 
expiration.  In  this,  as  in  all  similar  figures,  the  top  line  represents  time 
in  fifths  of  seconds. 


attract  immediate  attention.  Irregularity  of  a  very  similar 
kind  is  found  frequently  at  the  age  of  puberty,  and  it  is  also 
seen  on  rare  occasions  in  the  adult  (a  striking  example  of 
the  last  is  shown  in  Fig.  6). 

All  these  irregularities  are  of  vagal  origin. 


Sinus  arrhythmia. 


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14  Chapter  II. 

Sinus  irregularities  which  bear  no  relation  to  respiration. 

While  the  vagal  irregularities  of  heart  rhythm  generally 
show  a  respiratory  relation,  disturbances  of  similar  origin 
occur  where  there  is  no  association  between  the  changes  and 
the  several  acts  of  breathing.  These  disorders  of  the  heart 
mechanism  fall  into  three  main  categories.  They  are  : — 
(1)  Sudden  and  prolonged  cessation  of  the  whole  heart  beat, 
a  condition  so  rare  that  it  requires  but  a  passing  notice  in 
this  general  survey.  (2)  Phasic  variation  of  pulse  rate,  in 
which  a  retardation  and  subsequent  gradual  acceleration 
of  the  whole  heart  occurs;  the  change  is  spread  over  ten, 
fifteen  or  more  seconds  and  may  be  repeated  regularly  or 
may  occur  from  time  to  time  ;  it  is  associated  with  the 
administration  of  heavy  doses  of  drugs  of  the  digitalis  group, 
but  may  be  seen  apart  from  them  (Fig.  7)  ;  it  is  a  relatively 
uncommon  type  of  irregularity.  (3)  An  irregularity  of  the 
whole  heart  of  mild  degree,  in  which  shorter  and  longer 
pauses  are  mingled  indiscriminately.  It  is  not  infrequent, 
and  is  almost  always  combined  with  a  general  reduction 
of  pulse  rate.  It  may  be  found  in  quite  young  and  apparently 
healthy  children  (Fig.  8)  and  is  also  encountered  in  young 
adults  in  whom  no  other  cardiac  sign  is  apparent.  It  is 
specially  frequent  in  patients  who  have  rheumatic  heart 
disease  and  who  are  under  the  influence  of  digitalis  ;  it  is 
accentuated  when  the  heart  slows  after  it  has  quickened  in 
response  to  exercise. 

These  sinus  irregularities,  like  those  which  are  related  to 
respiration,  are  due  to  alterations  of  vagal  tone. 

The  recognition  of  sinus  irregularities. 

Sinus  irregularities  are  usually  recognised  with  ease. 
It  may  be  said  that  the  great  majority  of  pulse  irregularities 
which  occur  before  the  end  of  the  first  decade  are  of  this  kind, 


Sinus  arrhythmia.  15 

and  most  of  them  are  respiratory.  When  there  is  the 
definite  and  stated  relation  to  respiration,  no  further  evidence 
is  required  ;  in  most  instances  of  sinus  irregularity,  this 
relation  is  present,  but  if  it  is  absent,  it  becomes  established 
if  the  breathing  is  deepened  ;  a  gradual  waxing  and  waning 
of  rate  is  always  highly  suggestive,  if  not  conclusive.  The 
radial  beats  and  apex  pulsations  correspond  ;  the  heart 
sounds  are  simply  modified  according  to  the  incidence  of  the 
ventricular  contractions.  The  radial  beats  are  full,  and  the 
apices  of  the  several  pulsations  maintain  an  almost  constant 
height  in  arterial  curves  (Fig.  4,  5  and  8). 

The  irregularity  is  abolished  by  any  factor  which  notably 
increases  the  average  pulse  rate.  Thus  it  disappears  with 
exercise,  with  fever,  or  shortly  after  the  administration  of 
atropine. 

The  prognostic  significance  of  sinus  irregularities. 

The  commoner  forms  of  sinus  irregularity  (excluding  the 
prolonged  and  sudden  cessation  of  the  heart  beat  and  the 
true  phasic  variation  of  pulse  rate)  are  of  little  prognostic 
value.  They  are  so  frequently  found  in  patients  who  present 
no  other  sign  of  cardiac  disturbance,  either  at  the  original 
examination  or  subsequently,  that  they  are  to  be  regarded 
either  as  slight  exaggerations  of  a  normal  phenomenon 
(respiratory  irregularity)  or  as  evidences  of  a  mild  and  in- 
significant instability  of  tonic  inhibitory  nerve  action.* 
Their  importance  lies  chiefly  in  possible  confusion  with  other 
forms  of  heart  irregularity.  They  should  not  be  allowed  to 
influence  the  habits  of  those  who  exhibit  them  ;  neither  do 
they  suggest  or  require  any  special  therapeutic  measures. 


*  Occurring  in  children,  this  irregularity  has  obtained  an  exaggerated  and 
vmenviable  reputation,  on  account  of  its  supposed  relation  to  tuberculous 
meningitis. 


(      16     ) 


Chapter  III. 


HEART-BLOCK. 

Definition. 

An  abnormal  heart  mechanism,  in  which  there  is  a 
delay  in,  or  absence  of,  response  of  the  ventricle  to  auricular 

impulses. 

The  nature  of  heart-block. 

Under  normal  circumstances  the  ventricle  depends,  for 
its  stimulus,  upon  impulses  which  are  sent  down  to  it  from 
the  regularly  contracting  auricle.  Each  auricular  systole 
transmits  a  stimulus  to  the  ventricle  and  this  stimulus 
travels  from  auricle  to  ventricle  along  a  narrow  neuro- 
muscular tract,  the  auriculo-ventricular  bundle.  This  band 
of  tissue  starts  in  the  right  auricle  near  the  coronary  sinus 
and  proceeds  forwards  and  downwards  to  the  membranous 
septum  of  the  ventricle  (Fig.  1),  where  it  divides  into  two 
main  branches  on  either  side  of  the  septum.  The  main 
branches  subdivide  and  are  connected  to  the  ventricular 
musculature  through  the  complex  network  of  cells  named  after 
Purkinje.  The  sequence  in  which  the  chambers  of  the  heart 
contract  is  diagrammatically  illustrated  by  Fig.  9.  The  black 
rectangles  represent  auricular  (^4)  and  ventricular  (V)  systoles. 


Heart-block.  17 

When  from  any  cause  the  function  of  the  tissues  uniting 
auricle  and  ventricle  is  impaired,  a  disturbance  of  this 
sequential  contraction  is  engendered.  The  grades  of 
disturbance,  which  human  hearts  manifest,  are*  numerous. 

There  may  be  a  mere  prolongation  of  the  interval  which 
separates  the  commencements  of  auricular  and  ventricular 
systole  (the  As-Vs  interval,  as  it  is  termed).  Such  a  con- 
duction defect  is  illustrated  by  Fig.  10  ;  the  thin  lines  become 
more  oblique  in  the  diagram,  and  a  gap  is  left  between  the 
end  of  auricular  and  the  beginning  of  ventricular  systoles. 


Fig.  9.  Fig.   10. 

Fig.  9.  A  diagram  representing  the  action  of  the  normal  heart.  The  auricle 
contracts  first  and  transmits  an  impulse  (the  oblique  line)  to  the  ventricle. 
The  ventricle  responds  and  commences  to  contract  immediately  at  the 
cessation  of  auricular  systole. 

Fig.  10.  A  diagram  illustrating  the  earliest  stage  of  heart-block.  An 
interval  appears  between  the  end  of  auricular  and  the  commencement  of 
ventricular  contraction.  There  is  delay  in  the  transmission  of  the 
impulse  from  auricle  to  ventricle  (indicated  by  the  obliquity  of  the  line 
which  joins  the  rectangles  in  the  diagram). 

Where  the  grade  of  heart-block  is  higher,  the  ventricle 
may  fail  to  respond  to  occasional  auricular  impulses.  Such 
is  the  condition  when  "  dropped  beats  "  are  spoken  of.  This 
form  of  heart-block  is  rarely  a  simple  phenomenon  ;  it  is 
almost  always  complicated  by  variations  in  the  lengths  of 
As-Vs  intervals  over  the  period  of  disturbance.  The 
relation  of  chamber  contractions  may  be  studied  in  Fig.  11. 
A  "  dropped  beat  "  or  ventricular  silence  produces  a  pause 
of   exceptional   length   and   this   pause    breaks   the   natural 


18  Chapter  III. 

rhythm  of  the  ventricle.  Where  there  is  no  associated 
variation  in  the  As-Vs  intervals,  the  length  of  the  pause 
is  necessarily  equal  to  that  of  two  regular  pulse  beats.  But 
this  is  rarely  the  case  ;  the  "  dropped  beat  "  is  foreshadowed 
by  a  progressive  increase  of  the  preceding  As-Vs  intervals 
(cp.  Fig.  11,  1,  2  and  3).  Moreover,  the  As-Vs  interval 
which  follows  the  silence  is  generally  curtailed  (Fig.  11,  4). 
These  two  events  shorten  the  long  pause  and  consequently 
diminish  the  disturbance  of  the  ventricular  rhythm.  The 
exact  manner  in  which  the  changes  happen  is  of  importance 
and  requires  closer  study.  Consider  the  first  three  .4s-  Vs 
intervals  of  Fig.  11  ;  as  illustrated  by  the  obliquity  of  the 
lines,  the  interval  gradually  widens,  but  it  widens  in  a 
peculiar    manner.        The  •  increase    of    the    second    interval 


1 1 1 1 1 1 1 1 


i 


Fig.  11.  The  next  stage  of  heart-block,  to  which  the  term  "  dropped  beats  " 
is  applied.  Up  to  the  point  where  the  chief  disturbance  occurs,  the  gaps 
between  the  auricular  and  corresponding  ventricular  contractions  widen 
out.  The  impulses  travel  to  the  ventricle  with  increasing  difficulty.  The 
fourth  auricular  contraction  stands  isolated,  it  yields  no  response  ;  a 
ventricular  contraction  is  "  dropped."  Following  the  ventricular  pause, 
the  As-Vft  interval  is  short,  for  the  tissues  have  rested,  but  it  again 
widens  as  successive  cycles  follow. 


I'M 
i   i 


Fig.   12.     A  diagram  of  2  :  1  heart-block,  in  which  alternate  ventricular  beats 
are  "  dropped." 


Heart-block.  19 

over  the  first  is  greater  than  the  increase  of  the  third  over  the 
second.  The  result  is  a  decrease  of  the  interventricular 
period  directly  preceding  the  ventricular  silence.  The 
ventricle  quickens  to  the  point  of  the  disturbance.  The 
shortening  of  the  As-Vs  interval  following  the  pause,  and  the 
subsequent  prolongation  of  it,  produces  a  similar  quickening 
of  the  ventricle  after  the  disturbance.  The  primary  and 
secondary  accelerations  of  ventricular  rate,  before  and  after 
the  disturbance,  offer  a  very  helpful  clue  to  the  recognition 
of  many  cases  of  clinical  heart-block. 

As  the  grade  of  heart-block  rises,  and  ventricular 
silences  become  more  frequent,  relatively  simple  ratios  are 
established  between  the  auricular  and  ventricular  rates. 
When  the  ventricle  beats  at  only  half  the  rate  of  the 
auricle,  because  alternate  impulses  are  ineffective,  the  con- 
dition is  spoken  of  as  2  :  1  heart-block  (Fig.  12).  3:1  and 
4  :  1  ratios,  in  which  each  third  or  fourth  auricular  impulse 
alone  yields  a  ventricular  response,  are  sometimes  encountered, 
but  they  are  not  common. 

The  mechanisms  which  have  been  described  are  all 
included  under  the  term  "  partial  heart-block." 


I  I  I  I  I  I  I  I  I 
I     II     II     I 


Fig.  13.  A  diagram  of  complete  heart-block  or  dissociation.  Both  the 
auricle  and  the  ventricle  beat  regularly,  but  at  independent  rates.  The 
relative  positions  of  auricular  and  ventricular  contractions  are  very 
variable. 

c  2 


20  Chapter  III. 

The  final  grade  of  heart-block  is  reached  when  no 
impulses  are  transmitted  to  the  ventricle.  When  this 
happens,  the  ventricle,  having  completely  lost  the  controlling 
influence  of  the  auricle,  beats  in  response  to  a  slow  and 
regular  series  of  impulses  which  it  builds  up  intrinsically. 
In  "  complete  heart-block  "  or  "  dissociation  "  two  entirely 
separate  rhythms  are  maintained  ;  one  starts  in  and  controls 
the  auricle,  the  other  originates  in  and  controls  the  ventricle. 
The  first  has  the  usual  rate,  72  per  minute  or  thereabout, 
the  last  has  an  approximate  rate  of  30  to  the  minute. 
Though  both  are  regular,  the  rhythms  are  quite  independent 
(Fig.  13)  and  the  systoles  of  auricle  and  ventricle  fall  with 
very  varying  time  relations  to  each  other. 


Etiological  and  pathological  associations. 

Age.  Heart-block  may  occur  at  any  age.  It  has  been 
observed  in  the  newborn  child  and  at  almost  all  ages  into 
the  eighties  and  nineties.  Its  age  distribution  is  settled 
by  the  age  incidence  of  the  diseases  which  produce  it.  Thus, 
it  is  especially  prevalent  amongst  those  whose  hearts  have 
been  severely  damaged  by  rheumatic  fever  or  chorea, 
so  that  a  special  class  of  cases  is  grouped  between  the 
years  10  and  35.  Senile  affections  account  for  another 
large  group  of  patients  who  suffer  from  this  cardiac 
disturbance  ;  these  patients  are  elderly.  But  the  causation 
is  so  varied  that  no  age  is  exempt.  The  distribution  in  my 
own  series  has  been  as  follows  : — 


Age    10-20 

20-30 

30-40 

40-50 

50-60 

60-70 

70-8Q 

80-90 

Cases     7 

7 

5 

8 

3 

6 

5 

1 

Sex.     As  in  other  disturbances  of  the  cardiac  mechanism, 
heart-block  is  most  prominent  in  the  male  sex.       I   may 


Heart-block.  21 

illustrate  this  by  a  reference  to  my  own  series,  in  which  33 
are  males  and  9  are  females. 

Heredity.  A  single  instance  of  the  supposed  occurrence 
of  several  cases  of  heart-block  in  the  same  family  has  been 
reported,  but  has  not  been  substantiated.  It  is  highly 
improbable  that  heredity  plays  any  direct  part  in  the  affection. 

Relations  to  infective  disease.  Relatively,  heart-block 
is  not  infrequent  during  the  course  of  infective  diseases,  and 
of  these  I  believe  rheumatic  fever  holds  the  first  place  ; 
the  disturbance  is  usually  temporary.  The  exact  relation  of 
rheumatic  affections  to  acute  and  sub-acute  inflammatory 
lesions  of  the  heart  is  but  imperfectly  known,  but  there  is  a 
clear  connection  between  them.  A  number  of  instances  of 
heart-block  have  been  reported  during  the  course  of  severe 
rheumatic  fever  and  its  complications,  acute  endocarditis  and 
pericarditis.  It  is  probable  that  the  infection  of  the  heart  is 
rarely  limited  to  its  outer  or  inner  layer  ;  there  is  a  growing 
belief  that  the  middle  layer  or  myocardium  is  also  frequently 
involved.  My  own  experience  leads  me  to  think  that  heart- 
block  is  almost,  if  not  quite,  a  common  accompaniment  of 
acute  or  sub-acute  rheumatism  of  the  heart,  for  I  have  seen 
several  cases  recently  in  which,  during  the  course  of  rheu- 
matic fever  involving  the  valves  or  pericardium  or  both,  the 
patients  exhibited  dropped  beats  or  partial  heart-block  in 
its  several  grades.  In  other  instances,  temporary  heart- 
block  has  appeared  during  short  febrile  attacks  in  patients 
who  have  been  previously  affected  by  rheumatic  fever.  It  is 
certain  that  being  transient  it  is  often  overlooked. 

Of  other  acute  affections  which  should  be  mentioned  are 
those  of  the  more  active  pus  organisms,  and  also  those  of 
diphtheria,  influenza,  typhoid  and  pneumonia  ;  heart-block 
in    these    conditions    is    limited    to    infections    of    severity. 


22  Chapter  III. 

A  very  large  proportion  of  the  reported  cases  of  chronic 
heart-block  and  of  those  which  have  come  under  my  own 
observation,  have  belonged  to  two  groups  ;  the  disorder  has 
been  found  subsequent  to  single  or  repeated  attacks  of  rheu- 
matic fever,  or  has  been  the  direct  result  of  syphilis.  Whether 
of  rheumatic  or  syphilitic  origin,  heart-block  is  generally  but 
an  expression  of  a  widespread  affection  of  the  heart  muscle 
in  these  patients,  though  the  lesion  may  be  confined 
to,  or  may  fall  most  heavily  upon,  the  tissues  which  establish 
functional  connection  between  the  auricle  and  ventricle. 
In  a  fourth  of  the  cases  in  which  the  hearts  have  been  secured 
after  death  the  lesion  has  been  gummatous.  From  my  own 
series  of  38  cases,  4  gave  a  history  of  venereal  infection  and 
12  a  history  of  rheumatism. 

The  relation  of  heart-block  to  rheumatism  in  chronic 
heart  affections  is  a  peculiar  one.  The  heart-block  is  often 
dormant  or  is  detected  only  by  exact  instrumental  methods  ; 
it  is  often  unmasked  by  the  administration  of  drugs  of  the 
digitalis  group,  for  the  higher  grades  of  heart-block  are 
produced  from  the  lesser  by  these  poisons. 

Relation  to  chronic  degenerative  processes  of  more  obscure 
origin.  A  very  large  number  of  the  reported  cases  of  heart- 
block  have  been  in  elderly  people,  and  observation  has  shown 
that  the  damage  responsible  for  the  disturbance  has  been 
part  and  parcel  of  a  more  or  less  widespread  change,  either 
in  the  heart  itself,  or  in  the  heart  and  its  vessels.  A  number 
of  the  lesions  can  undoubtedly  be  traced  to  syphilis  or 
rheumatism,  but  the  cause  of  a  still  larger  number  is  obscure. 
Chronic  inflammation,  fibrosis,  atrophy,  calcification  or  fatty 
degeneration  of  the  tissues,  associated  or  unassociated  with 
disease  of  the  coronary  arteries,  are  amongst  the  most 
frequent  causes. 


Heart-block.  23 

Heart-block  as  a  result  of  digitalis  administration.  I  have 
already  referred  to  the  unmasking  of  dormant  heart-block 
in  rheumatic  heart  disease.  When  digitalis,  or  an  allied  drug 
such  as  strophanthus  and  squills,  is  given  in  toxic  doses  to 
young  patients  who  have  rheumatic  hearts,  it  is  not  uncommon 
to  observe  the  severer  grades  of  partial  heart-block  as  a  result. 
And  it  is  known  that  in  most  of  the  cases  which  react  in  this 
manner  a  slight  defect  in  the  conduction  of  impulses  from 
auricle  to  ventricle  was  present  before  the  drug  was 
taken.  The  added  effect  is  often  due  to  the  action  of 
digitalis  upon  the  vagus  nerve,  for  it  can  be  removed  by 
atropine. 

Heart-block  can  be  induced  in  experiment  by  stimulation 
of  the  vagus,  and  efforts  have  been  made  to  establish  a 
clinical  group  in  which  the  heart-block  is  attributable  to 
disturbance  of  innervation.  Up  to  the  present  time,  there 
is  no  very  clear  record  of  the  initiation  of  even  a  temporary 
disturbance  of  this  character  by  vagal  impulses  ;  though, 
as  I  have  stated,  a  pre-existing  tendency  may  be  exaggerated 
in  this  manner  ;  while  if  the  higher  grades  of  persistent 
heart-block  are  ever  due  to  derangement  of  vagus  action, 
such  a  causation  is  so  rare  that  it  scarcely  comes  within  the 
practical  field. 

Morbid  anatomy.  It  is  in  the  main  bundle,  or  in 
its  auricular  attachment,  that  the  lesions  responsible  for 
heart-block  have  been  described.  The  kind  of  lesion  has 
been  spoken  of  already.  Gummata,  chronic  inflammatory 
processes  and  their  accompaniments,  fibrosis,  atrophy,  and 
calcification  are  most  frequently  found.  Examples  of  tumours 
(fibroma  and  endothelioma)  affecting  these  special  tissues 
have  been  recorded. 

Ulceration  invading  the  bundle,  acute  inflammation 
evidenced  by  deposition  of  leucocytes,  or  parenchymatous 


24  Chapter  III. 

degeneration  of  the  bundle  are  the  common  lesions  in  hearts 
which  have  been  damaged  by  acute  infections. 


The  recognition  of  heart-block. 

The  disorders  of  the  heart's  mechanism  caused  by 
heart-block,  in  its  several  grades,  are  readily  recognised  by  the 
exact  graphic  methods  provided  by  the  polygraph  and 
galvanometer.  The  efficacy  of  these  instruments  and  the 
certainty  of  the  analysis  must  be  evident,  for  heart-block 
produces  derangement  of  sequence  in  the  contractions  of 
auricle  and  ventricle,  and  the  polygraph  and  galvanometer 
supply  separate  and  clear  records  of  the  systoles  of  upper  and 
lower  chamber.  Therefore,  a  comparison  of  the  onsets  of  the 
several  systoles  is  relatively  simple  when  these  recording 
devices  are  employed. 

But  I  speak  to  those  to  whom  the  special  method  is  not 
available,  and  I  hope  to  show  that  heart-block  can  be 
recognised  in  many  of  its  grades  by  simpler  means.  It  will 
be  necessary  to  treat  each  form  of  mechanism  separately  and, 
in  this  instance,  to  refer  especially  to  exact  measurement  of 
the  arterial  pulse  pauses.  In  many  forms  of  irregularity 
such  measurement  is  not  necessary,  though  it  may  be 
expedient  ;  in  the  disturbance  produced  by  heart-block  it  is 
often  essential. 

Often  the  earliest  manifestations  of  heart-block  consist 
in  a  widening  of  the  As-Vs  interval  (see  page  17)  ;  this  defect 
can  rarely  be  identified  by  ordinary  clinical  means  ;  yet 
it  may  be  responsible  for  two  physical  signs.  It  may  not  be 
known  to  everyone  that  auricular  systole  produces  a  distinct 
though  muffled  sound,  and  that  while  this  sound  is  inaudible 
when  the  heart's  mechanism  is  normal,  it  is  frequently  heard 
when  the  auricular  and  ventricular  systoles  are  sufficiently 


Heart-block.  25 

separated.  A  slight  widening  of  the  As-Vs  interval  may- 
lead  to  a  reduplication  of  the  first  heart  sound  ;  a  more 
pronounced  widening  may  result  in  a  double  second  sound, 
for  the  auricular  systole  may  fall  in  early  diastole. 

The  second  sign  is  confined  to  cases  of  mitral  stenosis  and 
is  of  similar  origin  ;  in  these  patients  the  systole  of  the  auricle 
is  the  cause  of  the  presystolic  murmur  which  characterises  the 
valve  lesion.  Contraction  of  the  auricle  at  an  abnormal 
instant  in  diastole  is  accompanied  by  a  murmur  and  thrill 
which  replace  the  customary  presystolic  events.  When  the 
pulse  is  regular,  apical  thrills  or  rough  murmurs,  confined  to 
mid-  or  early  diastole,  are  physical  signs  which  should  suggest 
not  alone  stenosis  but  also  the  beginning  of  heart-block. 

Single  dropped  beats  are  not  difficult  to  identify.  Take 
the  case  where  a  pulse,  which  seems  otherwise  regular,  is 
interrupted  by  an  occasional  pause  of  unusual  length,  while 
examination  of  the  apex  beat  reveals  neither  movement  nor 
sound  in  the  pause.  If  the  pause  is  not  associated  regularly 
with  the  phase  of  expiration  (see  page  12)  it  can  be  attributed 
to  a  failure  of  the  customary  response  of  ventricle  to  auricle. 
The  length  of  the  pause  in  radial  tracings  may  be  exactly 
equivalent  to  that  of  two  rhythmic  beats.  More  frequently 
(as  in  the  radial  pulse  tracing  of  Fig.  14)  it  is  distinctly  short 


Fig.  14.  A  pulse  curve  showing  "  dropped  beats."  The  arrows,  which 
represent  the  positions  of  the  regular  auricular  contractions,  have  been 
accurately  determined  in  this  and  subsequent  figures  by  means  of  poly- 
graphic  curves.  There  is  of  course  a  big  delay  between  the  auricular 
systole  and  the  pulse  beat.  The  heart  sounds  are  shown  diagrammatically. 
The  arrangement  of  the  pulse  beats  depends  upon  the  lengths  of  the  As-  Vs 
intervals  and  upon  the  failure  of  response  at  the  points  marked  by 
asterisks.  Note  the  widening  of  the  As-  Vs  intervals  and  accompanying 
increase  of  pulse  rate  before  and  after  each  dropped  beat. 


26  Chapter  III. 

of  this,  and  is  preceded  and  succeeded  by  slight  pulse  quicken- 
ing. The  nature  of  these  phenomena  has  been  considered 
already  (page  18),  and  the  mechanism  is  indicated  in  the 
present  figure  by  means  of  the  arrows  which  show  the  points 
at  which  the  regular  auricular  systoles  fall.  Responses  to  the 
auricular  contractions  marked  by  asterisks  have  failed. 


When  dropped  beats  are  more  frequent,  the  irregularity  takes  the  form 
of  that  seen  in  Fig.  15.  Here  each  third  or  fourth  impulse  miscarries, 
and  the  heart  and  pulse  beats  are  grouped  in  twos  and  threes.  Had  we  not 
the  termination  of  this  curve,  the  analysis  of  the  first  half  could  not  be  com- 
pleted, for  the  picture  is  identical  with  that  produced  by  premature  con- 
tractions. The  clue  to  the  true  interpretation  is  given  by  the  lengths  of 
pauses  1  and  3  ;  they  are  equal.  These  are  the  opening  beats  of  two  groups, 
the  first  of  two,  the  second  of  three  pulsations.  The  long  pause  which  follows 
each  group  is  of  constant  length  ;  it  has  been  produced  by  a  constant  mechan- 
ism. If  the  pulse  which  follows  the  first  group  were  attributable  to  pre- 
maturity of  pulse  beat  2,  a  similar  pause  would  be  expected  after  pulse  beat  4. 
It  does  not  occur,  and  we  recognise  in  3  and  4  the  acceleration  of  pulse  rate 
which  precedes  or  follows  an  unusual  pause  resulting  from  heart-block. 


Fig.    15.     Curves  of  heart's  apex  beat  and  pulse  from  a  patient  in  whom 
ventricular  responses  failed  frequently. 


2  : 1  heart-block  is  to  be  suspected  in  any  patient  in 
whom  the  ventricle  beats  regularly  and  where  the  rate  lies 
between  40  and  50  contractions  a  minute.  A  sudden  and  exact 
halving  of  ventricular  rate  is  always  most  suggestive.  2  :  1 
heart-block  is  usually  an  unstable  condition,  the  ventricle 
quickening  from   time   to   time,   and   these   changes  in   the 


Heart-block. 


27 


frequency  of  its  response  to  auricle  disclose  the  nature  of 
the  whole  disturbance. 


KadmL 


Fig.  1G.  Curves  of  heart's  apex  beat  and  pulse,  taken  during  the  passage 
of  the  mechanism  from  a  condition  of  frequent  "  dropped  beats  "  to 
2  :  1  heart-block.  The  rate  is  reduced  to  exactly  three-fourths  the 
original  at  the  change. 


¥       f     V     V     " 


v3A— ^i--^VYAA^^.H-^- 


t     •  * 


Fig.  17.  Curves  showing  the  interruption  of  a  period  of  2  :  1  heart-block 
by  a  single  response  of  the  ventricle  to  one  of  the  series  of  alternate 
impulses  which  usually  yield  no  ventricular  contraction. 


The  transition  between  2  :  1  heart-block  and  an  arrangement  previously 
studied,  namely,  the  loss  of  each  third  response,  is  shown  in  Fig.  16.  A 
bigeminal  or  coupled  action  of  the  ventricle  passes  over  into  a  slow  regular 
action.  The  features  which  proclaim  heart-block  in  this  curve  are  the  increase 
in  the  length  of  pause  from  a  to  b,  and  the  exact  reduction  of  rate  to  three- 
fourths.  The  lengths  of  the  several  pauses  are  understood  by  examining  the 
positions  of  the  auricular  systoles  which  have  been  indicated  by  arrows 
drawn  on  the  curve.  Systoles  2a,  4a,  5a,  6a  and  7a  do  not  affect  the  ventricle  ; 
and  where  the  ventricle  is  silent  an  unusually  lengthy  pause  is  found.  The 
arterial  pause  a  is  brief  as  compared  with  b  because  the  auricular  impulse 
4  takes  longer  to  reach  the  ventricle  than  does  impulse  5.  Disturbance 
of  a  2  :  1  period  is  shown  in  Fig.  17.  An  early  contraction  of  the  ventricle 
is  followed  by  a  pulse  pause  a  which  is  shorter  than  b  and  the  succeeding 
pauses.  The  reason  of  this  shortening  has  been  explained  in  the  description 
of  the  last  figure.  In  Fig.  17  heart-block  is  also  evidenced  by  the  fact  that 
the  total  duration  (c)  of  the  two  short  beats  is  equal  to  one  and  a  half  times 
the  duration  of  the  longer  beats  (period  d).  In  other  words  c  and  d  correspond 
to  three  auricular  cycles. 


28 


Chapter  III. 


In  mitral  stenosis  partial  heart-block  is  often  character- 
ised by  peculiarities  of  the  murmurs.  They  are  often 
extremely  complex.  Where  2  :  1  heart-block  is  present  two 
thrills    and    two    diastolic    murmurs    may    accompany    each 


Ape* 


iu«B     In.,       9    I 


wild      *•• 


Fig.  18.  Arterial  and  apex  curves  from  a  case  of  mitral  stenosis,  while  the 
mechanism  passes  from  a  condition  of  dropped  beats  to  2  :  1  heart-block. 
Note  the  arrangement  of  the  diastolic  murmurs  and  their  dependence 
upon  auricular  contractions. 


Fig.  19.  Apex  and  radial  curves  in  a  case  of  complete  heart-block.  The 
heart  sounds  are  modified  by  the  auricular  contractions,  which  are 
faintly  audible.  Where  auricular  and  ventricular  contractions  begin 
together  the  first  sound  is  exaggerated.  The  pure  auricular  sounds  are 
shown  as  dots. 


ventricular  cycle.  The  meaning  of  the  phenomenon  will  be 
obvious  if  it  is  remembered  that  the  thrill  and  harsh  murmur 
of  mitral  stenosis  are  produced  by  auricular  systole  and  that 
in  2  :  1  block  the  auricle  contracts  twice  as  frequently  as  the 
ventricle.       A   more   complex   arrangement  of  murmurs  is 


Heart-block.  29 

shown  in  Fig.  18.  The  ventricle  beats  at  first  in  couples, 
and  at  such  times  the  murmur  occurs  before  the  first  and  after 
the  second  sound  of  the  first  beat  of  a  couple  ;  the  second 
beat  of  the  couple  is  accompanied  by  no  murmur,  for  the 
single  auricular  contraction  in  its  neighbourhood  falls  with 
that  of  the  ventricle  and  no  blood  is  forced  through  the 
stenosed  orifice.  Over  the  last  portion  of  the  curve  2:  1 
heart-block  is  present,  and  each  cycle  is  accompanied  by 
presystolic  and  early  diastolic  murmurs. 

In  complete  heart-block  the  action  of  the  ventricle  is 
phenomenally  slow  ;  almost  all  hearts  which  beat  at  rates  of 
35  and  under  are  affected  in  this  manner.  The  rhythm  is 
generally  quite  regular.  Each  ventricular  beat  is  accom- 
panied by  a  first  and  second  sound,  and  in  addition  very 
faint  muffled  sounds  are  heard  in  the  long  diastoles.  These 
are  due  to  auricular  systoles.  A  sign  which  is  characteristic, 
and  often  present,  is  a  modification  of  the  first  and  second 
heart  sounds  from  beat  to  beat.  When  the  auricular  and 
ventricular  contractions  begin  together,  the  first  sound  is 
intensified,  and  when  they  fall  almost  together  the  first  or 
second  sound  may  be  reduplicated  (Fig.  19).  Evidences  of 
the  relatively  rapid  auricular  contraction  are  generally  seen  in 
the  neck  ;  small  and  regular  pulsations  (Fig.  20,  a  waves)  are 
shown  by  the  jugular  veins  between  the  beats  of  the  carotid 
(c  waves).  From  time  to  time  a  prominent  venous  pulsation 
(Fig.  20,  a/c)  accompanies  the  intensified  first  heart  sound, 
when  auricular  systole  coincides  with  that  of  the  ventricle  and 
when  as  a  consequence  the  blood  cannot  be  driven  forward  out 
of  the  auricle.  A  periodic  waxing  and  waning  of  the  venous 
pulsations,  independent  of  respiration,  is  always  highly 
suggestive  of  the  condition.  Traces  of  auricular  pulsations 
upon  the  arterial  curves  are  also  evident  in  most  of  the 
patients  from  whom  full  pulse  excursions  can  be  obtained 


30 


Chapter  III. 


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Heart-block.  31 

(Fig.  21).  Where,  as  in  the  accompanying  figure,  the  little 
waves  on  the  downstrokes  of  the  regular  pulse  beats  show  a 
gradual  and  orderly  change  of  position,  moving  steadily  away 
from  the  succeeding  radial  upstroke,  the  presence  of  complete 
heart-block  is  certain. 

Effects  on  the  circulation  and  the  general  symptomatology . 

The  symptoms  presented  by  patients  with  heart-block 
are  divisible  into  two  groups.  On  the  one  side  are  the  symp- 
toms which  are  the  special  appurtenance  of  the  condition 
itself,  and  on  the  other  are  those  which  result  from  co- 
existing disease  in  other  portions  of  the  heart.  For  disease 
is  rarely  limited  to  the  bundle,  and  generally  heart-block  is 
but  a  local  manifestation  of  a  more  widespread  process  ; 
the  local  lesion  is  often  accidental.  The  effects  of  a  lesion 
which  transects  the  bundle  differ  from  those  of  a  similar  lesion 
in  another  portion  of  the  musculature  in  one  chief  respect  ; 
the  damage  gives  rise  to  obvious  disturbance  ;  there  is  no 
second  strand  which  may  fulfil  the  functions  of  that  which  is 
destroyed,  whereas  a  defect  in  the  general  mass  of  muscle  is 
hidden  by  the  response  of  the  remaining  tissue.  As  in  disease 
of  the  nervous  system,  where  large  areas  of  tissue  may  be 
lost  without  gross  signs  of  damage,  but  where  a  minute 
morbid  focus  in  a  given  situation  gives  rise  to  obvious  and 
profound  disturbance  ;  so  it  is  with  the  heart.  It  is  necessary 
to  emphasise  the  fact  that  heart-block  is  usually  an  indication 
of  a  far  graver  condition  than  simple  transection  of  the  bundle; 
it  is  a  sign  of  wide  or  universal  invasion  of  the  myocardium. 

The  symptoms  which  result  from  affections  of  the 
whole  heart  musculature  do  not  lie  within  the  scope  of  this 
book  ;  but  it  is  important  to  recognise  that  the  presence  of 
heart-block  demands  an  exhaustive  study  of  the  subject  in 
whom  it  appears  ;    in  all  instances  special  attention  should 


32  Chapter  III. 

be  directed  to  the  fitness  or  otherwise  of  the  heart  as  a  whole. 
And  this  caution  is  not  limited  to  heart-block,  it  applies  to 
all  departures  from  the  normal  mechanism. 

The  special  symptomatology  of  heart-block  may  be 
conveniently  approached  from  two  standpoints. 

Heart-block  of  high  grade  is  accompanied  by  a  reduction 
of  the  rate  of  the  heart  beat,  often  to  a  half  its  former  rate. 
What  is  the  effect  of  this  retardation  of  heart  rate  upon  the 
circulation,  and  what  are  the  results  of  the  lessened  nervous 
control  of  rate  which  often  accompanies  it  ?  It  is  certain 
that  thereby  a  serious  burden  is  imposed  upon  the  efficiency  of 
the  heart  as  a  pump  ;  but  nothing  is  more  remarkable  than 
the  accommodation  of  the  cardiovascular  system  to 
conditions  which  diverge  widely  from  the  normal  ones. 
Dissociation  of  auricles  and  ventricles,  and  the  consequent 
establishment  of  a  slow  ventricular  rhythm,  is  followed  by 
some  degree  of  ventricular  hypertrophy.  Undoubtedly,  this 
increase  in  the  mass  of  the  ventricular  muscle  compensates 
in  a  measure  for  the  loss  of  co-ordination  and  of  the  natural 
rates.  During  the  long  diastoles  the  blood  is  squeezed  from 
arteries  to  veins  and  a  low  diastolic  blood  pressure  results  ; 
but  the  blood  pours  equally  fast  from  veins  to  heart,  whose 
efficient  chambers,  receiving  the  extra  load,  expel  it  into  the 
arteries.  Fullness  of  pulse  and  high  systolic  pressure  (170-200 
mm.  Hg.)  consequently  characterise  the  arterial  system  when 
in  persistent  heart-block  there  is  no  lack  of  healthy  cardiac 
tissue.  As  evidences  of  the  adaptability  of  the  circulation 
as  a  whole  to  the  new  conditions,  I  may  cite  the  case  of  a 
patient  in  whom,  judging  from  the  signs  and  symptoms,  the 
damage  to  the  muscle  mass  is  but  little.  The  patient,  a  man 
of  33  years,  is  known  to  have  had  a  heart  rate  of  30  to  35, 
with  occasional  accelerations  to  48,  for  13  years.  He  is  the 
subject  of  complete  heart-block.  There  is  a  little  hypertrophy 
of  the  heart,  but  no  subjective  symptoms.     He  leads  a  very 


Heart-block.  33 

active  business  life,  and  passed  in  the  street  would  be  judged 
a  perfectly  normal  and  healthy  individual.  There  is  no 
circulatory  embarrassment,  even  after  strenuous  exertion  ; 
he  prides  himself  upon  his  "  sprinting  "  power  and  has  raced 
during  the  past  few  years.  An  instance  of  this  kind  offers 
a  partial  answer  to  the  original  questions  ;  the  slow  pulse 
of  heart-block  and  the  absence  of  regulation  of  rate  do  not 
disable  an  otherwise  healthy  heart  from  performing  its  full 
work.  In  hearts  more  profoundly  affected,  the  extra  burden 
is  less  readily  borne,  but  in  these  it  is  not  easy  to  dissociate 
the  effects  of  the  new  mechanism  from  those  of  disease  of 
the  remaining  muscle. 

In  the  second  place,  heart-block  is  responsible  for  a 
group  of  symptoms  which  arise  as  a  direct  result  of  excessive 
slowing.  Reduction  of  pulse  rate  beyond  certain  limits,  or 
the  cessation  of  the  arterial  flow  for  a  certain  time,  is  accom- 
panied by  grave  disorders  of  nutrition,  and  the  brain  is  an 
early  and  anxious  plaintiff.  The  patient,  who  exhibits 
marked  pulse  slowing  in  conjunction  with  fits,  falls  into  the 
category  of  Adams-Stokes'  syndrome.  The  higher  grades 
of  heart-block,  whether  of  persistent  heart-block  in  which 
ventricular  responses  are  frequently  missed  (2:1,  3:1 
ratios,  etc.),  or  of  complete  dissociation,  are  frequently 
accompanied  by  temporary  periods  of  excessive  pulse  slowing 
or  by  cessation  of  the  ventricular  systole  for  prolonged 
intervals.  The  cause  of  the  change  in  ventricular  rate,  for 
the  auricles  continue  to  beat  at  the  usual  or  at  an  enhanced 
rate,  is  not  fully  understood,  and  I  do  not  propose  to  consider 
it  further.  The  symptoms  presented  by  the  patient  are 
intimately  dependent  upon  the  degree  of  heart  slowing  or 
upon  the  duration  of  isolated  periods  of  asystole.  When 
the  pulse  falls  to  8  or  20  beats  per  minute,  unconsciousness 
supervenes  ;  suspension  of  the  mental  functions  is  also 
produced  by  a  single  period  of  asystole  of  from  3  to  7  seconds 


34  Chapter  III. 

duration.  Patients  who  suffer  from  the  higher  grades  of 
heart-block  commonly  give  a  history  of  brief  attacks  of 
giddiness,  fainting,  temporory  loss  of  consciousness  and  its 
dependent  accidents.  Seen  in  mild  attacks,  the  subject 
of  them  is  pulseless  and  momentarily  pale.  In  severer 
seizures,  where  the  pulse  ceases  for  15  seconds  or  more,  there 
are  additional  phenomena.  The  blood  is  dammed  back  in 
the  venous  system,  increasing  pallor  has  cyanosis  added  to 
it,  the  breathing  deepens  and  becomes  stertorous  ;  twitching 
of  the  face  and  upper  limbs  eventually  occurs.  The  con- 
vulsive fit  rarely  spreads  beyond  the  named  area,  but  it 
may  become  more  generalised.  Urine  is  not  passed,  neither 
is  the  tongue  bitten  during  the  attacks.  In  most  cases  the 
condition  is  readily  recognised  by  the  absence  of  signs 
of  ventricular  activity  and  by  the  presence  of  rapid 
undulations  in  the  veins  of  the  neck,  signifying  activity  of 
the  right  auricle.  Unexpected  death  is  a  by  no  means 
uncommon  accident  amongst  the  affected,  but  considering 
individual  attacks  it  is  rare.  Death  occurs  after  a  period  of 
status  epilepticus  in  a  number  of  the  patients,  and  the  status 
consists  of  repeated  seizures  of  the  forms  described. 

As  a  rule  the  patient  has  no  warning  of  an  impending 
syncopal  or  epileptic  attack  ;  though  on  occasion  he  or  his 
medical  attendant  may  be  informed  of  the  approaching 
danger  by  a  change  in  the  heart's  action,  for  example,  by  the 
occurrence  of  further  ventricular  slowing.  The  sensations 
of  the  patient  at  the  commencement  of  long  seizures  are 
usually  similar  to  those  accompanying  a  brief  cessation  of 
the  heart  beat,  and  consequently  do  not  properly  constitute 

an  aura. 

The  prognosis. 

Heart-block  in  itself  does  not  kill  ;  those  who  suffer  or 
have  suffered  from  it  mostly  die  with  the  usual  symptoms  of 
general  heart  failure.     Let  me  be  clearly  understood  in  this 


Heart-block.  35 

statement.  Heart-block  and  the  Adams-Stokes'  syndrome 
are  not  synonymous  terms  ;  the  majority  of  patients  who 
exhibit  heart-block  never  have  fits.  Lesser  grades  of  heart- 
block  are  common  in  conjunction  with  rheumatic  heart 
disease  and  as  a  rule  they  produce  no  symptoms. 
Moreover,  the  disturbed  mechanism  is  not  of  necessity 
directly  fatal  even  in  chronic  heart-block  of  high  grade. 

The  prognosis  in  heart-block  has  to  be  dealt  with  from 
several  points  of  view.  In  the  first  instance,  let  us  consider 
the  milder  grades  of  heart-block,  such  as  are  associated  with 
rheumatic  heart  disease  (prolonged  As-Vs  intervals  or 
"  dropped  beats  ").  Where  such  heart-block  is  persistent , 
there  are  usually  a  number  of  physical  signs  in  addition  to 
those  dependent  upon  the  heart  mechanism  ;  they  are  the 
signs  of  heart  disease,  muscular  or  valvular,  and  in  its  several 
and  universally  recognised  forms.  Heart-block  is  often  the 
least  prominent  symptom  in  these  cases  ;  they  are  often  to  be 
classed  as  mitral  stenosis.  The  only  question  that  I  raise 
is  as  to  the  manner  in  which  heart-block  affects  the  prognosis 
in  these  cases.  It  should  be  regarded  as  an  evidence  of 
myocardial  damage,  not  necessarily  limited  to  the  bundle, 
but  probably  diffused  throughout  the  heart.  My  experience 
of  such  cases  is  that  they  are  serious  ;  in  fact,  most  of  those 
I  have  seen  are  dead,  though  they  did  not  die  of  heart-block. 
But  temporary  heart-block  of  mild  grade  is  not  uncommon 
during  the  febrile  attacks  to  which  rheumatic  heart  subjects 
are  liable  ;  it  occurs  also  in  pneumonia  and  typhoid.  The 
appearance  of  this  abnormal  mechanism  is  of  great  importance, 
for  it  is  often  the  sole  sign  which  indicates  that  the  myo- 
cardium has  been  damaged.  Whenever  it  complicates  an  acute 
infection  it  consequently  increases  the  gravity  of  the  prognosis ; 
at  the  same  time  it  should  be  understood  that  the  normal 
mechanism  is  usually  recovered.  Occurring  as  an  accom- 
paniment of  fever  in  a  patient  who  has  rheumatic  heart 

D  2 


36  Chapter  III. 

disease,  it  should  be  regarded  as  an  outward  sign  of  an  isolated 
injury  which,  if  often  repeated,  eventually  so  weakens  the 
muscle  that  life  is  no  longer  supported. 

Where  the  higher  grades  of  heart-block  are  present,  the 
prognosis  is  based  upon  two  chief  considerations.  The 
general  evidence  of  the  integrity  and  fitness  of  the  muscle  as  a 
whole  should  be  weighed  first.  The  fits,  especially  their 
frequency  and  severity,  are  next  taken  into  account  :  a 
number  of  the  patients  are  free  from  them  ;  others  are  in 
constant  peril  ;  and  it  is  not  easy,  nay  it  is  often  impossible, 
to  predict  the  ultimate  effects  of  syncopal  attacks  or  severer 
crises  in  a  given  case.  Those  patients  especially  who  have 
progressive  lesions,  and  those  in  whom  partial  is  eventually 
converted  to  complete  and  permanent  dissociation,  must 
pass  through  a  time  of  particular  danger  ;  for,  during  the 
passage  from  one  mechanism  to  the  other,  fits  are  very 
common  and  the  period  of  passage  may  not  be  a  short  one. 
It  is  useful  to  remember  also  that  those  who  have  partial 
heart-block  are  more  prone  to  fits  than  those  in  whom  the 
obstruction  is  complete.  Uncertain  in  both  incidence  and 
effects,  the  fits  always  dictate  a  cautious  prognosis. 

Regarded  in  its  entirety,  persistent  heart-block  of  high 
grade  is  a  grave  condition.  It  is  usually  complicated,  and 
then  a  few  years  generally  close  the  scene.  Nevertheless,, 
some,  and  especially  the  younger  patients,  survive  for  many 
years,  in  comparative  and  absolute  comfort.  They  are  those 
in  whom  the  mass  of  heart  muscle  is  comparatively  healthy 
and  in  whom  fits  are  rare  or  absent. 

The  treatment. 

Persistent   heart-block   of   the   milder  forms   requires   no 

immediate    treatment,    but    is    an    indication    for    repeated 

examination  of  the  patients  who  show  it.     As  such  patients 

usually  require  treatment  for  the  general  condition  of  the 


Heart-block.  37 

heart,  constant  supervision  is  not  difficult.  They  often 
require  digitalis  medication,  and  this  will  frequently  increase 
the  grade  of  block.  But  the  increase  of  block  should  not 
deter  digitalis  administration  for  the  relief  of  dilatation, 
dropsy  or  other  symptoms  ;  nor  is  it  in  itself  detrimental ;  the 
drug  or  its  allies  may  be  given  without  restraint  and  often 
beneficially. 

When  the  abrupt  onset  of  partial  heart-block  is  observed,  it 
is,  as  I  have  said,  an  index  of  active  mischief.  The  patient 
should  lie  up  or  remain  in  bed  and  should  be  thoroughly 
searched  for  the  provocative  cause,  which,  when  found,  is 
attended  to.  The  acute  infections  are  suitably  treated. 
Rheumatic  patients  are  treated  with  salicylates,  and  scrupulous 
attention  is  paid  to  the  hygiene  of  the  mouth  and  throat.  If, 
after  the  subsidence  of  remaining  symptoms,  the  block 
remains  and  persists  for  several  weeks,  the  patient  is  treated 
along  the  lines  indicated  in  the  previous  paragraph.  Heart- 
block  in  itself  does  not  call  for  rest  in  bed  or  other  interference, 
though  a  suspicion  of  an  active  or  progressive  lesion  does. 

The  higher  grades  of  heart-block  are  usually  chronic  and 
stationary  and  the  habits  of  the  patient  should  be  governed 
by  his  general  fitness.  Most  patients  of  this  class  are  up 
and  about,  and  are  able  to  undertake  many  of  their  ordinary 
duties  ;  yet  it  is  only  in  exceptional  instances  that  real 
bodily  activity  is  either  possible  or  permissible.  Here 
again  a  suspicion  that  the  lesion  is  active  or  progressive 
calls  for  rest  and  careful  watching.  A  history  or  sign  of 
syphilis  constitutes  an  imperative  demand  for  thorough  and 
appropriate  treatment,  and  in  some  cases  success  has  attended 
the  administration  of  mercurials  arid  iodides. 

All  those  who  have  fits  should  be  warned  of  the  danger 
which  they  run  from  falls  during  fits  if  they  do  not  appreciate 
it  fully.  Not  a  few  have  lost  their  lives  by  falling  heavily 
and  suffering  mortal  injury.     In  many  cases  the  fits  occur  in 


136524 


38  Chapter  III. 

groups,  and  additional  precautions  will  be  required  until 
such  attacks  cease.  Most  patients  have  brief  warnings  of  the 
onset  of  unconsciousness,  and,  if  advantage  is  taken  of  them, 
less  risk  is  incurred. 

A  careful  inquiry  for  causes  predisposing  to  the  fits  may 
elicit  a  history  of  gastro-intestinal  disturbance  or  over- 
exertion, upon  which  it  is  well  to  act. 

For  the  fit  when  it  is  present,  I  know  of  no  remedy 
which  is  of  avail  to  increase  the  pulse  rate  and  restore  the 
unconscious  patient.  A  number  of  drugs  have  been 
administered  with  this  end  in  view,  and  the  list  includes 
oxygen,  strychnia,  strophanthine,  digitalin  and  amyl 
nitrite.  They  appear  to  have  no  appreciable  effects. 
Atropine  is  said  to  have  abolished  fits  in  isolated  instances. 
As  a  rule  it  is  contra-indicated. 


(     39     ) 


Chapter  IV. 


PREMATURE    CONTRACTIONS. 

Definition. 

Responses  of  the  heart  to  new  and  isolated  impulses 
formed  in  the  musculature  ;  contractions  which  occur  before 
the  anticipated  time  and  which  consequently  disturb  the 
normal  order  of  the  heart's  mechanism. 

The  nature  of  premature  contractions* 

A  clear  and  full  appreciation  of  an  abnormal  heart 
mechanism  can  be  attained  only  by  those  who  are  perfectly 
familiar  with  its  normal  action.  The  orderly  sequence  of 
muscle  movements,  which  constitute  the  normal  heart  beat, 
is  propagated,  as  I  have  already  stated,  from  a  single 
impulse  born  in  the  sino-auricular  node.  The  contraction, 
starting  from  the  mouth  of  the  superior  vena  cava,  travels 
rapidly  through  the  auricle,  reaches  the  auriculo- ventricular 
node  and  traverses  this  node  and  the  bundle  which  is  its 
continuation  ;  it  is  distributed  in  an  orderly  manner  amongst 
the  mass  of  ventricular  fibres  in  which  it  ends.  The  normal 
rhythm  of  the  heart  consists  of  a  regular  sequence  of  such 
beats,  so  that  auricular  and  ventricular  contractions  fall  with 
the  proper  time  relations  to  each  other.  Each  stimulus 
elaborated  at  the  sino-auricular  node  requires  a  certain  time 

*  I  use  the  term  premature  contraction  in  preference  to  "  extrasy stole," 
a  name  which  has  been  and  still  is  employed  to  designate  the  same  abnormal 
beat. 


40  Chapter   I  V. 

of  preparation,  and  this  time  of  preparation  is  very  constant 
under  definite  and  given  circumstances.  It  is  relatively  long, 
reaching  nearly  two-thirds  of  a  second  when  the  heart  is 
beating  at  a  normal  rate.  Indeed  it  is  the  time  of  impulse 
preparation  which  controls  the  rate  of  a  normally  beating 
heart.  A  second  characteristic  of  physiological  impulse 
formation  is  regular  repetition.  Each  impulse  belongs  to  a 
regular  or  rhythmic  series. 

The  premature  or  pathological  contraction  differs  from 
the  physiological  in  two  fundamental  respects  The  impulse 
which  gives  rise  to  it  is  formed  at  a  phenomenally  rapid  rate. 
It  is  to  this  quality  that  the  pathological  contraction  owes 
its  prematurity.  The  absence  of  a  definite  tendency  for  the 
pathological  impulse  to  repeat  itself  constitutes  its  second 
distinctive  feature,  and  upon  this  character  the  usual  isolation 
of  the  pathological  contraction  depends.  Premature 
contractions  originate  abruptly,  and  may  spring  from  the 
auricle,  from  the  ventricle,  or  from  the  tissues  which  unite 
these  two  contractile  structures.  For  ordinary  clinical 
purposes  it  suffices  if  we  remember  the  two  chief  classes  of 
premature  beat,  the  auricular  and  the  ventricular. 

If,  while  the  heart  chambers  are  beating  in  a  normal  and 
sequential  manner,  a  pathological  impulse  arises  in  the 
ventricle,  the  ventricular  beat  which  it  awakens  will  fall  before 
the  anticipated  point  in  the  rhythmic  series  ;  whence  comes 
the  term  "  premature  contraction."  It  disturbs  the  sequence 
of  ventricular  contractions  in  a  definite  manner.  Excepting 
the  premature  impulse,  the  ventricle  is  absolutely  dependent 
for  its  stimuli  upon  the  impulses  which  descend  to  it  from  the 
auricle.  Consequently,  after  the  disturbance  produced  by  a 
single  premature  beat,  the  ventricle  rests  until  a  rhythmic 
auricular  impulse  reaches  it.  If  the  accompanying  diagram 
(Fig.  22)  is  studied,  it  will  be  seen  that  for  the  first  three 
cycles  the  ventricle  follows  the  auricle  in  contraction  ;    a 


Premature  Contractions.  41 

premature  beat  (p)  is  then  interposed  and  as  a  consequence  the 
next  auricular  impulse,  represented  by  the  broken  line,  arrives 
while  the  ventricle  is  already  in  a  state  of  contraction.    Being 


Fig.  22.  A  diagrammatic  representation  of  the  disturbance  produced  by 
a  premature  ventricular  contraction  (p).  The  auricle  beats  regularly 
throughout.  The  ventricle  responds  to  six  auricular  impulses. 
The  impulse  of  the  central  auricular  systole  is  lost,  for  it  falls 
while  the  ventricle  is  in  premature  systole.  The  abnormal  origin 
of  the  ventricular  beat  is  indicated  by  the  break  in  its  centre. 
Note  the  equality  in  the  lengths  of  /periods  a  and  b.  c  is  the 
compensatory  pause. 


in  contraction  the  ventricle  shows  no  response,  its  muscle 
is  in  the  "  refractory  "  state.  The  dominance  of  auricular 
impulses  is  reasserted  during  the  succeeding  cycle.  Thus, 
the  disorder  is  controlled  by  the  fundamental  heart  rhythm 
which  proceeds,  unheedful  of  the  disturbance.  The  ven- 
tricular contractions,  subsequent  to  the  disturbance,  fall  at 
points  which  may  be  accurately  anticipated  ;  the  period  of 
the  disturbance  (b)  is  exactly  equivalent  to  the  length  of  two 
complete  cycles  of  the  normal  rhythm  (a).  The  pause  which 
follows  the  premature  ventricular  beat  is  long  ;  the  ventricle 
is  waiting.  The  length  of  the  pause  (c)  is  such  as  to 
compensate  for  the  brevity  of  the  pause  which  precedes, 
consequently  it  is  spoken  of  as  the  "  compensatory  pause." 
When  a  premature  impulse  originates  in  the  auricle 
the  order  of  events  is  different.  The  premature  contraction 
of  the  auricle,  which  it  calls  forth,  is  followed  by  a  similar 


42  Chapter  I  V. 

and  parallel  disturbance  in  the  ventricle  (Fig.  23),  for  the 
ventricle  responds  to  each  auricular  contraction  wherever 
such  contractions  are  placed  in  a  series.  In  all  but  exceptional 
instances  too,  there  is  a  disturbance  of  the  fundamental  heart 

Mill 

a  b 

Fig.  23.  A  diagrammatic  representation  of  a  premature  auricular  con- 
traction. The  auricular  rhythm  is  disturbed  by  the  abnormal  auricular 
beat  (p)  ;  the  disturbance  in  the  ventricular  rhythm  is  parallel,  for 
each  auricular  systole  yields  a  ventricular  response.  The  rhythm  of  the 
whole  heart  is  dislocated,  the  period  a  is  longer  than  the  period  &■. 


rhythm  :  the  premature  contraction  (p)  is  followed  by  a  long 
pause,  but  the  whole  period  of  the  disturbance  (b)  is  not 
equivalent,  as  in  the  case  of  the  premature  ventricular  beat,, 
to  two  full  cycles  of  the  normal  rhythm  (a). 

Etiological  and  pathological  relations. 

Age.  Premature  beats  have  been  recorded  at  all  ages 
from  a  few  weeks  to  old  age.  During  the  first  decade  they 
are  extremely  rare.  Their  incidence  in  an  age  table  is 
actually  heaviest  between  50  and  70  years  ;  if  the  age 
distribution  of  the  populace  is  considered  in  conjunction 
with  this  fact,  it  becomes  evident  that  essentially  they  are  a 
phenomenon  of  advancing  years. 

Age  distribution  of  premature  beats  in  112  cases. 

Age  0-10    10-20   20-30   30-40   40-50   50-60    60-70    70-80    80-90   90-100- 

Auricular      024442  6  101 

Ventricular  2         13  8  9         14         20         18  4  0  0 

2         15         12         13         18         22         24  5  0  1 


Premature  Contractions.  A3 

Sex.  Premature  contractions  are  much  commoner  in 
men  than  in  women.  In  129  subjects  the  sex  distribution 
was  as  follows  : — 


Sex 

Male. 

Fern 

Auricular 

20 

12 

Ventricular 

65 

32 

85  44 

Associated  conditions  and  provocative  factors.  It  should 
be  remembered  that  any  statistics  compiled  to  show  the 
relations  of  premature  contractions  to  associated  conditions 
and  infections,  suffer  from  a  defect.  Those  cases  which  exhibit 
frequent  and  persistent  premature  beats  preponderate  in 
the  tables  ;  for  under  these  circumstances  they  are  conspicuous, 
while  if  they  are  scarcer  they  may  often  fail  to  attract  atten- 
tion. It  is  probable  that  the  majority  of  people  who  live 
to  middle  life  or  advanced  years  are  affected  in  this  manner 
at  some  time  or  another.  Amongst  patients  who  attend 
out-patient  departments  or  are  admitted  to  the  wards  of 
general  hospitals,  frequent  and  persistent  premature  con- 
tractions are  most  common  in  those  who  exhibit  definite 
symptoms  and  signs  of  cardiac  disease.  They  are  often 
found  in  association  with  aortic  incompetence  and  mitral 
stenosis  ;  an  even  larger  number  of  curves  are  collected  from 
patients  who  present  signs  of  degenerate  heart  muscle,  as 
evidenced  by  dilatation  and  S3^mptoms  of  muscle  insufficiency 
in  the  absence  of  gross  valve  lesions.  In  yet  another 
large  group  of  patients,  no  evidence  of  functional  impairment 
of  the  heart,  leaving  the  irregularity  out  of  consideration, 
can  be  discovered. 

Premature  auricular  contractions. 


Cardiac  group. 

Remainder. 

Myocardial  degeneration 

12 

Bronchitis  and  emphysema  . 

2 

Mitral  stenosis 

5 

Pulmonary  tuberculosis 

2 

Aortic  stenosis 

2 

Dyspepsia 

1 

Lumbago 

1 

• 

Exophthalmic  goitre  .  . 

1 

Apparently  healthy     . . 

4 

19  11 


44 

Chapter 

IV. 

Premature  ventricular  contractions. 

Cardiac  group. 

Remainder. 

Myocardial  degeneration 

24 

Tuberculosis  (lungs  and  pleura)        5 

Aortic  disease 

12 

Bronchitis  and  emphysema 

2 

Mitral  stenosis 

13 

Gallstones          .  . 

Angina  pectoris 

7 

Gangrene  of  toes  (senile) 

Bright's  disease  and  granulai 

Epilepsy 

kidney 

5 

Lipoma  of  neck 

Arteriosclerosis 

3 

Fractured  skull 

Acute  endocarditis 

2 

Abdominal  tumour 

Aneurism 

1 

Exophthalmic  goitre  .  . 
Gastric  ulcer 
Dyspepsia 

Apparently  healthy  otherwise       8 

67  24 

Of  the  factors  which  appear  to  be  predominantly 
associated  with  them,  gross  lesions  of  the  heart  stand  first. 
Otherwise  an  inquiry  into  the  habits,  history  and  state  of  the 
patients  throws  but  an  obscure  light  upon  the  causation.  A 
history  of  rheumatic  infection  is  certainly  common,  it  was 
present  in  one-third  of  the  cases  in  my  series.  In  young 
adults,  excessive  tobacco  smoking  is  recognised  as  an  exciting 
cause  of  their  temporary  appearance.  Digitalis  and  its 
allies  are  not  uncommonly  responsible,  when  the  patient  is 
under  the  full  influence  of  these  drugs.  There  are  also 
clinical  associations  between  premature  contractions,  raised 
arterial  pressure  and  digestive  disturbances,  but  these  are 
not  fully  understood  at  the  present  time. 

Many  things  affect  the  frequency  of  premature  con- 
tractions. Fatigue,  subsequent  to  exertion,  is  provocative 
in  those  who  are  predisposed.  The  influence  of  heart  rate 
is  especially  noteworthy.  Hearts  beating  at  100  per  minute 
and  over  are  not  often  disturbed,  and  premature  contractions 
are  very  rare  when  the  heart  rate  exceeds  120.  Fever 
usually  rids  the  pulse  of  this  form  of  irregularity,  and  so 
also  does  any  other  cause  which  notably  accelerates  the  pulse 
rate.  Thus  they  are  abolished  during  exercise  and  for  a 
short  period  afterwards,  but  during  the  period  of  slow  heart 
action  which  often  follows  exercise,  they  are  frequent.   As  we 


Premature  Contractions.  45 

shall  subsequently  see,  this  knowledge  may  often  be  used 
advantageously  to  induce  premature  beats  in  patients  pre- 
disposed to  them.  Suspension  of  respiration  for  a  period 
compatible  with  comfort  often  suffices.  The  pathological 
beats  are  in  evidence  either  in  the  apnceic  stage  or  shortly 
after  the  resumption  of  respiration.  No  factor  is  more 
potent  than  posture.  Patients,  who  exhibit  numerous 
premature  contractions  while  standing,  may  soon  lose  them 
in  recumbency,  and  this  despite  a  slight  decrease  of  heart 
rate  in  the  last  position.  In  other  patients,  pressure  upon 
the  abdomen  may  abolish  them. 

The  recognition  of  premature  contractions. 

The  work  accomplished  by  premature  beats  is  small, 
because  the  periods  of  rest  that  precede  them  are  short. 
They  may  or  may  not  raise  the  aortic  valves.  Accompanying 
the  premature  beat,  a  feeble  pulsation  or  a  prolonged  pause 
is  noted  in  the  arterial  pulse  ;  auscultation  reveals  early 
first  and  second  sounds  when  the  aortic  valves  are  forced, 
but  only  an  isolated  and  premature  first  sound  if  the  ven- 
tricular pressure  fails  to  top  the  arterial.  The  consequent 
grouping  of  sounds  in  threes  and  fours  is  comprehended  when 
the  nature  and  degree  of  the  corresponding  arrhythmia  are 
discerned.  The  commonest  arrangements  of  pulsations  and 
sounds  are  described  in  the  following  paragraphs,  and  are 
illustrated  by  the  accompanying  diagram  and  tracings. 

In  the  succeeding  paragraphs  I  have  sub-grouped  the 
symptoms  according  as  the  premature  beat  (a)  raises  or  {($) 
fails  to  raise  the  aortic  valves. 

1.  When  a  systole  of  a  regularly  beating  ventricle  is 
replaced  by  a  premature  beat,  this  abnormal  contraction  is 
accompanied  by  an  early  apex  thrust  and  by  (<*)  a  weak 
arterial  wave  and  two  extra  sounds,  which  together  with 
those  of  the  preceding  rhythmic  beat  form  a  group  of  four 


Chapter   I  V 


Fig.  24.  A  diagram  showing  common  disturbances  of  the  arterial  pulse  and 
heart  sounds  when  premature  ventricular  contractions  are  present. 
(a)  Normal  rhythm  ;  (b)  Occasional  premature  beat,  which  affects  arterial 
pressure  ;  (c)  Occasional  premature  beat,  which  fails  to  affect  arterial  pressure  ; 
id)  Premature  beat  replacing  each  third  normal  beat  and  affecting  arterial 
pressure;  (e)  Premature  beat  replacing  each  third  normal  beat  and  failing  to 
affect  the  arterial  pressure  ;  (/)  Premature  beat  replacing  each  second  normal 
beat  and  affecting  the  arterial  pressure  ;  (g)  Premature  beat  replacing  each 
second  normal  beat  and  failing  to  affect  arterial  pressure.  The  heart  sounds 
occur  in  groups,  and  the  groups  are  of  four  or  three,  according  as  the  aortic 
valves  are  raised  or  remain  at  rest  when  the  premature  beat  occurs. 


Premature  Contractions.  47 

{Fig.  24  b  and  25)  ;  or  by  (ft)  an  intermission  in  the  arterial 
pulse  and  one  extra  sound,  forming  with  the  sounds  of  the 
preceding  rhythmic  beat  a  group  of  three  (Fig.  24  c). 

2.  When  each  third  beat  of  the  regular  ventricular 
rhythm  is  replaced  by  a  premature  beat,  we  find  a  grouping 
of  the  apex  thrust  in  threes,  of  which  the  third  beat  in  each 
group  is  premature.  The  arterial  beats  (a)  are  grouped  in 
threes,*  with  groupings  of  the  apical  sounds,  so  that  two 
normal  heart  sounds  alternate  with  a  group  of  four  sounds 
(Fig.  24  d)  ;  or  (ft)  are  paired  with  grouping  of  the  apical 
sounds,  so  that  two  normal  heart  sounds  alternate  with  a 
group  of  three  sounds  (Fig.  24  e  and  30). 

3.  Premature  beats  which  alternate  with  rhythmic 
beats  give  rise  to  pairing  of  the  apical  thrusts  (Fig.  27,  28,  32), 
and  to  (a)  pairing  of  arterial  beats  of  which  the  second  stroke 
is  weak,  and  to  groupings  of  heart  sounds  in  fours  (Fig.  24  / 
and  29)  ;  or  to  (ft)  halving  of  the  rate  of  the  arterial  pulse, 
and  heart  sounds  in  groups  of  threes  (Fig.  24  g  and  28). 

The  differentiation  of  premature  auricular  and  ventricular 
beats  is  not  always  possible  without  full  instrumental 
examination. 

Where  an  occasional  premature  beat  occurs,  the  indica- 
tions of  its  ventricular  origin  are  as  follows  :  (a)  There  is  no 
disturbance  of  the  fundamental  heart  rhythm.  The  presence 
of  this  phenomenon  may  sometimes  be  elicited  in  feeling  the 
radial  pulse  by  anticipating  the  points  at  which  the  rhythmic 
beats,  following  the  disturbance,  ought  to  fall  to  carry  on  the 
original  rhythm  ;  but  it  is  usually  more  easy  to  identify 
instances  of  disturbance  of  the  rhythm  than  to  exclude 
them  by  this  method.  A  strip  of  radial  curve  alone  is  almost 
always  sufficient  to  distinguish  one  from  the  other  ;  in  the 
instance  of  the  premature  ventricular  beat  the  full  period 

*  Premature  beats  may  also  be  responsible  for  groups  of  three  arterial 
beats  when  they  replace  each  fourth  rhythmic  beat  (Fig.  26). 


48 


Chapter  I  V 


■  i— ■■  w wwm  >»<»i<»»»hii»^»j» 


Af** 


•         V  i 

Fig.  25.     Apex  and  radial  curves,  showing  a  single  premature  ventricular 
contraction   a  =  b. 


*"V     V    "V      VV      V     X     '»>"'»»      V     V      »     V     y     »      ■!■■■■'      tf     V      V  •  )•*  \f     *      *     v~*v— v- 


R«2.ial 


■■■i      via  ■- 

Fig.  26.  Radial  curve  and  heart  sounds  in  a  case  in  which  premature 
ventricular  contractions  replace  each  fourth  normal  beat.  Tha 
premature  beats  fail  to  affect  the  pulse. 


RaxAuJ 


«...  I       In,  I       Ik.  I        In.  III.  I  li„t'ln  In.  I  lb 


MinnriiiiiiiiiiiiiiMMiriiitiiiiiiiU'iinriniiiimmiiiiiiirT 


Fig.  27  and  28.  Apex  and  radial  curves  and  heart  sounds.  The  normal 
mechanism  passes  into  one  in  which  premature  ventricular  contractions 
replace  alternate  normal  beats.  Fig.  27  is  from  a  case  in  which  mitral 
regurgitation  was  present.     In  Fig.  28,  interval  a  =  b. 


At** 


Fig.  29.  Premature  ventricular  contractions  replacing  each  second  normal 
beat.  The  heart  sounds  are  grouped  in  fours  ;  the  pulse  is  of  the  form 
termed  pulsus  bigeminus. 


Premature  Contractions.  49 

of  the  disturbance  is  equal  to  two  normal  cycles  (Fig.  25). 
In  the  instance  of  the  premature  auricular  beat  the  full 
period  is  less  (Fig.  31).  (b)  There  is  a  prominent  jerk  and 
swelling  of  the  veins  of  the  neck  (Fig.  30)  at  the  time  of 
occurrence  of  the  premature  ventricular  beat.  This  is  brought 
about  in  the  following  fashion.  The  ventricular  beat,  falling 
prematurely  as  it  does,  usually  coincides  with  a  rhythmic 
auricular  contraction,  so  that  the  two  heart  chambers  are 
in  systole  together  (see  Fig.  22).  As  a  consequence  of  this 
simultaneous  contraction,  the  auricle  fails,  for  a  single  cycle, 
to  empty  itself  into  the  ventricle,  and  pumps  the  blood  back 
into  the  veins.  (c)  By  synchronism  of  the  premature 
ventricular  beat  with  the  rhythmic  auricular  contraction,  the 
corresponding  first  sound  is  often  exaggerated. 

Where  the  premature  beat  follows  pairs  of  normal  beats  or  alternates 
with  normal  beats,  signs  b  and  c  may  be  present,  but  a  is  usually  valueless 
unless  a  transition  from  a  period  of  disturbance  to  a  period  of  normal  rhythm 
is  graphically  recorded  (as  in  Fig.  28  and  32).  A  comparison  can  then  be 
instituted  between  the  lengths  of  the  disturbed  and  undisturbed  heart  cycles. 
Thus,  in  Fig.  28  the  long  pauses  are  exactly  twice  the  length  of  the  short  ones  : 
a  is  equal  to  b  ;  premature  contractions  arising  in  the  ventricle  have  created 
an  exact  halving  of  pulse  rate.  In  Fig.  32  the  pulse  following  the  premature 
contraction  is  not  compensator}^ ;   a  is  longer  than  b  (see  Fig.  23). 

The  effect  of  premature  beats  upon  the  auscultatory 
signs,  when  murmurs  are  present,  are  manifold  ;  yet  most  of 
them  can  be  foretold  if  the  general  principles  are  grasped. 
A  systolic  mitral  murmur  will  be  found  with  the  premature 
as  well  as  with  the  rhythmic  beat  (Fig.  27),  but  it  is  usually 
short  and  may  be  absent.  At  the  base  in  aortic  disease, 
a  systolic  or  diastolic  murmur  is  present  when  the  premature 
beat  raises  the  aortic  valves  (Fig.  33).  On  the  other  hand, 
in  mitral  stenosis,  a  presystolic  mitral  murmur  is  absent 
whether  the  premature  beat  is  auricular  or  ventricular,  but 
in  the  former  instance,  it  is  often  replaced  by  a  presystolic 
sound.  The  absence  of  the  presystolic  murmur  in  the  case 
of  the  auricular  beat  is  attributable  either  to  weakness  of  the 
premature  contraction  or  to  its  coincidence  with  the  preceding 
ventricular  systole. 


50 


Chapter  I  V. 


Fig.  30.  Curves  from  the  neck  and  radial  artery.  Premature  ventricular 
contractions  replace  each  third  normal  beat,  but  do  not  affect  the  pulse. 
An  exaggerated  first  sound  and  a  prominent  wave,  easily  visible  in  the 
neck,  accompanied  each  premature  beat ;  these  phenomena  result  from 
simultaneous  contraction  of  auricle  and  ventricle. 


Fig.  31.     Apex  and  radial  curves  showing  occasional  premature  auricular 
contractions  ;   a  is  greater  than  b, 


<iin)ni»iii  iiiiliii>r)nn 

_/tn r\A—DJ\ 


Fig.  32.  A  ':  bigeminy  "  or  coupling  of  heart  beats,  resulting  from  premature 
auricular  contractions,  passing  into  the  normal  rhythm ;  a  is  greater 
than  6. 


Ape* 


j\yVv/vi7VV\AyV\_ 


!>..        ■      I'     ■      It... 


Ra.<W 


Fig.  33.  A  bigeminy,  resulting  from  premature  auricular  contractions. 
The  beats  are  paired  in  apical  and  radial  curves.  Aortic  regurgitation 
was  present. 


Premature  Contractions.  51 

More  complex  heart  sounds  are  heard  in  instances  where 
a  premature  beat  raises  the  pulmonary,  but  not  the  aortic 
valves,  as  sometimes  happens  ;  the  second  pulmonary  sound 
occurs,  but  the  second  aortic  sound  is  absent.  This  pheno- 
menon has  been  erroneously  ascribed  to  hemisystole,  the 
presence  of  the  second  sound  of  the  right  heart  and  the 
absence  of  that  of  the  left  heart  being  taken  as  evidences 
of  activity  and  quiescence  of  the  respective  ventricles. 

The  subjective  phenomena  which  accompany  premature 
contractions. 

In  a  very  large  number  of  those  affected,  the  disturbances 
of  heart  rhythm  pass  unnoticed.  On  the  other  hand  pre- 
mature beats  are  not  an  uncommon  cause  of  what  patients 
term  "palpitation."  The  symptom  is  more  prominent  in 
young  subjects,  especially  those  of  female  sex  and  those 
afflicted  by  nervous  instability.  When  numerous,  they 
sometimes  occasion  actual  distress  ;  by  calling  attention  to 
the  heart,  they  often  induce  anxiety.  The  sensations 
experienced  are  exaggerated  by  depression  of  the  general 
health,  by  fatigue  and  by  emotion.  They  are  often  more 
noticed  after  the  patient  retires  for  the  night,  after  excessive 
smoking,  after  a  heavy  meal,  or  after  exertion. 

As  a  general  rule  the  premature  contraction  itself  passes 
unperceived  ;  the  long  pause  which  follows  awakens  a  sense 
of  uneasiness  or  oppression  in  the  chest,  or  a  feeling  of 
"  void,"  while  the  succeeding  contraction  of  the  heart  is 
accompanied  by  consciousness  of  shock  to  the  chest  wall  and 
frequently  by  a  feeling  of  gripping  in  the  throat.  Patients 
in  whom  these  sensations  are  vivid  sometimes  swallow, 
cough,  or  inspire  as  soon  as  they  experience  them.  When  a 
number  of  premature  beats  succeed  each  other  at  short 
intervals,  and  consciousness  of  them  is  marked,  anxiety  may 
be  profound,  and  faintness,  coldness  of  the  extremities  and 
«ven  sweating  may  result. 

E    2 


52  Chapter  I  V. 

The  prognosis  and  treatment. 

It  should  be  clearly  understood  that,  in  speaking  of  the 
prognostic  value  of  premature  beats,  I  speak  of  these  beats 
without  reference  to  the  conditions  with  which  they  are 
associated.  That  when  frequent  and  persistent,  they  often 
accompany  grave  affections  of  the  heart  will  be  evident  from 
a  study  of  the  tables  already  given  ;  but  this  fact  does  not 
materially  affect  the  question  before  us.  The  associated 
lesions  give  prognostic  indications  of  their  own  ;  our  inquiries 
are  as  to  whether  a  heart,  which  presents  no  other  sign,  can 
be  regarded  as  healthy  and  as  to  whether,  in  the  case  of  an 
unhealthy  heart,  the  prospect  has  an  added  gloom. 

It  must  be  admitted  that  all  such  beats  are  decided 
evidence  of  a  pathological  condition  and  that  the  pathological 
process  has  its  seat  in  the  tissues  of  the  heart.  The  presence 
of  premature  contractions  is  an  indication  of  disturbance  of 
cardiac  nutrition,  whether  temporary  or  permanent,  but  it  is 
an  aspect  that  should  not  be  allowed  undue  prominence. 
A  number  of  people  are  temporarily  affected  by  premature 
beats  which  do  not  reappear,  while  the  heart  manifests  no 
sign  of  further  damage,  either  at  the  time  or  afterwards.  In 
such  instances  it  is  impossible  to  suppose  that  the  disturbance 
of  the  cardiac  function  has  been  more  than  transient  or  that 
the  nature  of  it  has  been  serious.  Observations  and  inquiry 
also  teach  that  they  may  be  present  constantly  and  for  long 
periods,  and  that  those  who  manifest  them  may  do  so  from 
an  early  to  a  good  old  age,  such  patients  never  showing  any 
other  sign  or  symptom  of  cardiac  disability.  It  may  be  said 
therefore,  that  in  themselves  premature  beats  cannot  be 
regarded  as  evidences  of  serious  involvement  of  the  heart 
muscle,  although  such  involvement  is  often  found  in 
conjunction   with   them. 

The  question  can  be  regarded  from  another  standpoint. 
The  premature  contractions,  when  present  and  frequent,  must 


Premature  Contractions.  53 

inevitably  increase  the  work  of  the  heart,  but  the  amount  of 
the  added  burden  is  not  easy  to  ascertain.  It  is  probably 
not  weighty,  for  where  the  muscle  is  evidently  compromised 
and  frequent  premature  contractions  occur  periodically, 
little  change  in  the  condition  of  the  patient  can  be  detected 
from  time  to  time,  and  serious  embarrassment  of  the 
circulation  as  a  direct  result  of  them  is  only  suspected  on 
rare  occasions. 

Modern  observations  therefore  tend  to  minimise  the 
significance  of  these  beats  ;  in  fact  it  has  been  taught  that 
they  may  be  neglected  in  the  forecast.  My  own  standpoint 
is  a  more  guarded  one.  Premature  contractions  constitute 
and  bear  witness  to  defects  ;  there  is  the  mechanical  imper- 
fection and  there  is  the  evidence  of  altered  cardiac  nutrition  ; 
and  the  more  frequent  the  interruptions,  the  greater  the 
degree  of  such  defects.  Moreover,  single  premature  beats 
testify  to  the  presence  of  a  process  which  may  lead  to  cardiac 
irregularities  of  a  more  serious  nature.  They  may  be 
precursors  of  grave  conditions  which  are  considered  in 
subsequent  chapters.  Premature  beats,  true  paroxysmal 
tachycardia,  auricular  flutter  and  fibrillation  have  a  common 
pathological  basis  ;  they  are  one  and  all  the  outcome  of  new 
impulse  formation  in  the  heart.  While  it  is  true  that  the 
majority  of  hearts  which  show  premature  contractions  may 
never  exhibit  profounder  derangements,  it  is  also  true  that 
these  occur  for  the  most  part  in  hearts  in  which  single 
interruptions  have  been  common  ;  it  follows  that  of  hearts 
seen  to-day,  some  of  which  show  premature  contractions  and 
some  of  which  show  none,  the  incidence  of  grave  irregularities 
will  in  later  years  be  greater  in  the  former  than  in  the  latter. 

I  may  summarise  in  the  statement  that,  while  premature 
contractions  have  unquestionably  a  relatively  insignificant 
import,  as  compared  to  many  forms  of  cardiac  irregularity, 
entire  neglect  of  their  presence  is  not  advisable.     Although 


54  Chapter  I  V. 

their  detection  should  not  be  allowed,  in  itself,  to  cripple  or 
hamper  the  patient  who  is  the  subject  of  them,  a  re-examina- 
tion of  such  cases  from  time  to  time  is  recommended. 

The  first  standpoint  of  treatment  is  already  indicated. 
The  presence  of  premature  beats  does  not  call  for  a  limitation 
of  bodily  exercise  ;  it  should  not  prejudice  the  vocation  or 
pastime  of  the  patient.  Restrictions  are  necessitated  only 
where  other  signs  render  them  advisable,  or  where  some 
particular  act  or  occupation  is  definitely  known  to  originate 
symptoms  of  a  distressing  kind.  The  anxiety  to  which  the 
beats  conduce  in  some  subjects  may  be  materially  allayed  by 
reassurance.  No  drugs  are  known  which  influence  their 
prevalence  ;  digitalis  as  a  direct  measure  is  contra-indicated. 
The  symptoms  are  usually  masked  or  considerably  modified 
by  the  bromides  administered  in  doses  of  from  fifteen  to 
thirty  grains  or  more  a  day  ;  and  these  drugs  are  especially 
useful  in  tiding  a  nervous  or  excitable  patient  over  a  period 
of  disturbance. 


(     55     ) 


Chapter  V. 


SIMPLE    PAROXYSMAL    TACHYCARDIA. 

Definition. 

Paroxysmal  tachycardia  is  a  term  which  has  been  and 
still  is  applied  to  several  distinct  phenomena.  It  will  be  of 
material  assistance  at  present  if  I  restrict  my  description  to 
the  simple  form  and  define  it  as  a  condition  in  which  from 
time  to  time  the  normal  mechanism  is  abruptly  submerged 
in  rapid  contractions  of  the  muscle  in  response  to  a  series  of 
new,  rhythmic  and  pathological  impulses  varying  in  rate  from 
110  to  200  per  minute.* 

The  nature  of  simple  paroxysmal  tachycardia. 

It  has  been  stated  that  the  normal  pacemaker  of  the 
heart  lies  at  the  union  of  the  superior  cava  and  right  auricle. 
The  usual  rate  at  which  the  rhythmic  impulses  proceed  from 
this  focus  is  72  per  minute  in  the  adult.  If  a  new  centre  of 
impulse  formation  develops  in  any  portion  of  the  heart  wall, 
and  this  centre  initiates  muscle  responses  at  a  rate  surpassing 
that  of  the  normal  rhythm,  then,  while  it  is  active,  the  new 
centre  dominates  the  movements  of  the  whole  heart.  Such 
are  the  paroxysms  which  we  are  about  to  study  ;  they  consist 
of  sudden  accelerations  of  heart  rate  in  response  to  the 
awakening  of  new  pathological  impulses.     The  paroxysms 

*  In  so  defining  it  I  have  purposely  excluded  all  accelerations  of  normal 
or  sinus  rhythm,  for  these  are  dependent  upon  innervation.  I  have  also 
excluded  two  forms  of  tachycardia,  which  are  closely  related  to  that  described 
in  the  present  chapter  ;  one,  which  is  regular,  but  in  which  the  auricular  rate 
exceeds  200  per  minute  (see  Chapter  VI)  ;  the  other,  which  is  irregular 
(see  Chapter  VII). 


56  Chapter    V. 

may  be  regarded  both  clinically  and  pathologically  as  formed 
essentially  of  a  regular  series  of  premature  beats.  The  new 
impulses  are  elaborated  in  a  single  focus,  whence  the  regularity 
of  the  series,  and  this  focus  lies,  usually  or  always,  at  a  point 
which  is  removed  from  the  pacemaker.*    Fig.  34  opens  with 


Fig.  34.  A  diagrammatic  representation  of  a  short  paroxysm  of  premature 
auricular  beats  :  a  paroxysm  of  tachycardia.  The  abnormal  auricular  beats 
are  broken  in  their  centres.  Each  yields  a  ventricular  response.  The  first 
abnormal  beat  occupies  the  same  position  in  relation  to  preceding  events 
as  does  that  of  Fig.  23.  The  short  paroxysm  ends  in  a  pause  y.  y  is 
longer  than  x. 

three  normal  heart  beats,  and  the  fourth  auricular  contraction 
(p)  is  premature.  Up  to  this  point  the  diagram  is  identical 
with  that  shown  in  Fig.  23f  ;  it  differs  from  the  earlier  picture 
in  the  repetition  of  the  abnormal  contraction,  five  such  beats 
following  each  other  in  rapid  and  regular  succession.  In  each 
instance  the  ventricle  responds.  The  paroxysm  terminates, 
and  its  end  is  marked  by  a  pause  (y)  which  is  longer  than  the 
pause  (x)  intervening  between  the  beats  of  the  normal 
rhythm  J  ;  its  length  is  generally  that  of  the  pause  which 
succeeds  an  isolated  premature  contraction  (see  Fig.  23). 

*  A  statement  which  is  based  upon  the  findings  of  electro-cardiographic 
curves. 

f  In  both  diagrams  I  have  broken  the  auricular  rectangle,  to  emphasise 
the  abnormal  birthplace  of  the  pathological  contractions. 

J  The  interval  (x)  has  been  deliberately  chosen  at  the  onset  of  the 
paroxysm,  because  the  restored  rhythm  of  the  old  pacemaker  is  often  slow 
for  a  few  cycles.  For  simplicity  this  retardation  is  not  figured  but  it  will  be 
referred  to  again  at  a  later  stage. 


Simple  Paroxysmal  Tachycardia.  57 

How  important  a  clear  pathological  conception  of  this 
disturbance  is,  will  be  evident  :  for  the  nerve  control  of  a 
new  centre  of  impulse  formation  is  not  known  from  analogy  ; 
as  a  matter  of  fact  the  new  rhythms  show  only  limited 
subordination  to  vagal  and  sympathetic  control. 

The  sites  in  which  the  new  rhythms  develop  are 
numerous  ;  the  abnormal  focus  is  generally  seated  in  the 
auricle,  and  the  usual  sequence  of  contraction  is  consequently 
maintained  in  the  heart  chambers  ;  but  it  may  be  ventricular, 
and  the  auricle  then  responds  inversely  to  the  ventricular 
beats.  The  chief  features  of  the  mechanism  will  be  sufficiently 
impressed  by  a  closer  examination  of  the  commoner  auricular 
variety.  The  diagram  exhibits  a  paroxysm  of  five  beats,  and 
this  short  series  permits  the  display  of  both  onset  and  offset. 
Actually  the  attack  may  last  a  few  seconds  or  a  week  or  more  ; 
whatever  its  length  the  mechanism  is  constant,  but  the 
symptoms  vary  with  the  duration. 

The  total  range  of  rate  in  this  the  simple  form  of 
paroxysmal  tachycardia  is  from  110  to  200  per  minute  ; 
•during  most  paroxysms  the  heart  contracts  140  to  190  times 
per  minute. 

Etiological  and  pathological  relations. 

Age.  Paroxysmal  tachycardia  occurs  at  all  ages  after 
the  first  decade.  The  actual  age  limits,  so  far  as  observed 
cases  are  concerned,  are  6-74.  In  my  own  series,  which 
comprises  45  cases,  the  age  distribution  is  as  follows  : — 


Age 

10-20 

20-30 

30-40 

40-50 

50-60 

60-70 

70-80 

•Cases 

4 

11 

7 

7 

7 

6 

3 

A  single  instance  has  been  recorded  in  a  child  of  6  years. 
The  highest  incidence  is  between  20  and  30. 

Sex.     In  my  series  30  males  and  15  females  are  included. 
That  is  to  say,  the  disorder  is  a  good  deal  more  frequent  in 


58 


Chapter    V. 


men  than  in  women.  This  proportion  is  in  fair  agreement 
with  other  records,  though  perhaps  the  male  element  is  less 
predominant  in  the  whole  number. 

Heredity  has  been  blamed,  but  the  evidence  is  insufficient 
to  show  that  it  has  any  direct  influence. 

Relations  to  infective  disease.  In  quite  half  the  cases  no 
history  of  previous  illness,  other  than  perhaps  children's 
ailments,  can  be  traced.  Rheumatic  fever  is  the  only 
infection  which  is  at  all  common.  Occasional  instances 
appear  to  have  followed  immediately  upon  malaria,  measles 
and  scarlet  fever  ;   a  few  of  the  patients  have  been  syphilitic. 

Associated  conditions.  Most  cases  of  paroxysmal  tachy- 
cardia are  found  to  have  no  sign  of  valve  lesion,  and  in  a 
large  number  of  the  patients  there  is  little  or  no  evidence  of 
dilatation   during  the  intervals  between  the  paroxysms. 

Nevertheless  a  number  of  them  show  a  limitation  in  the 
field  of  cardiac  response  and  become  breathless  with  slight 
exertion.  Taking  dilatation,  in  the  absence  of  valve  lesion, 
undue  breathlessness  upon  exertion  and  the  subsequent 
development  of  more  serious  signs  of  cardiac  failure  as 
evidences  of  degeneration  of  the  myocardium,  I  have  placed 
nine  of  the  patients  in  a  corresponding  group.  The  only 
valve  lesion  which  figures  prominently  is  mitral  stenosis, 
being  present  in  ten  of  my  cases. 


Paroxysmal  tachycardia  and  associated  conditions. 

Mitral  stenosis 

Myocardial  degeneration 

Arterial  disease  (with  and  without  angina 

Aneurism  (thoracic) 

Renal  disease  and  cardiac  dilatation 

Early  pulmonary  tuberculosis 

No  other  signs 


10 
10 
4 
1 
3 
1 
16 


45- 


Simple   Paroxysmal  Tachycardia.  59 

Factors  promoting  attacks.  Exertion  or  emotional  dis- 
turbance are  the  chief  excitants  of  attacks  in  those  predisposed 
to  them,  and  the  number  of  instances  in  which  the  history 
tells  of  paroxysms  evoked  in  these  ways  is  remarkable.  The 
induction  of  a  first  attack  by  unaccustomed  effort  is  often 
responsible  for  their  hasty  assignment  to  overstrain,  but  it  is 
questionable  if  strain  is  ever  the  complete  story ;  more 
probably,  damaged  or  perverted  muscle  is  in  all  cases  the 
underlying  mischief.  Flatulence,  other  digestive  disturbances, 
and  especially  the  assumption  of  certain  postures,  are  amongst 
the  chief  remaining  excitants  of  crises. 

Morbid  anatomy.  In  the  instances  in  which  examination 
has  been  possible  after  death,  the  most  prominent  and 
frequent  lesions  have  been  in  the  walls  of  the  heart.  Fibrosis, 
pallor,  friability,  atrophy  and  interferences  with  the  arterial 
supply  are  the  chief  naked  eye  changes  recorded.  In  a  few 
cases  of  tachycardia  nerve  lesions  have  been  found,  but  their 
association  with  the  specific  condition  with  which  we  now 
deal  is  more  than  doubtful. 

The  recognition  of  simple  paroxysmal  tachycardia. 

A  heart  rate  of  180  or  more  in  an  adult  is  usually  the 
result  of  pathological  impulse  formation,  and  especially  is  this 
the  case  where  a  heart  lesion  is  known  to  be  present.  The 
rate  of  the  ventricidar  beating  is  preserved  when  the  patient 
passes  from  the  upright  to  the  recumbent  position  ;  it  is  rarely 
altered  by  more  than  a  few  beats  per  minute  even  when  he  is 
maintained  in  a  supine  position  for  considerable  periods  of 
time.  A  physical  sign  of  the  utmost  diagnostic  importance 
may  be  noted  at  the  onset  or  offset  of  an  attack,  the  increase 
and  decrease  in  rate  at  these  times  is  absolutely  abrupt.  In 
patients  who  are  conscious  of  the  rapid  heart  action,  but  in 
whom  the  offset  and  onset  cannot  be  observed,  the  sudden 


60  Chapter    V. 

change  at  the  beginning  or  ending  of  the  attack  can  usually 
be  elicited  by  careful  questioning. 

Other  physical  signs  which  may  be  present  are  of 
importance,  though  their  significance  is  not  so  great.  A 
prominent  and  palpable  pulsation  in  the  veins  of  the  root  of 
the  neck  is  often  present ;  it  may  be  almost  aneurysmal 
in  force.  The  arterial  pulse  is  frequently  irregular  in 
force,  and  at  the  first  examination  may  give  an  erroneous 
impression  of  an  irregularly  beating  ventricle.  No  obser- 
vations are  more  unreliable  than  counts  of  pulse  rates  taken 
in  the  ordinary  manner  during  the  paroxysms  ;  they  should 
always  be  checked  at  the  apex  beat,  either  by  palpation  or 
auscultation.  The  heart  sounds  are  tic  tac  in  character  and 
murmurs  which  may  have  been  noticed  on  previous  occasions 
usually  disappear  while  the  heart  rate  is  raised.  The  last  sign 
is  of  value  in  mitral  stenosis,  in  which  such  attacks  are 
relatively  common  ;  for  the  presystolic  murmur  is  abolished. 
When  a  rough  presystolic  murmur  is  lost  by  a  patient 
who  develops  an  accelerated  and  regular  heart  action,  the 
disappearance  of  the  murmur  is  generally  attributable  to  the 
onset  of  an  abnormal  rhythm.  In  patients  who  suffer 
periodically  from  tachycardia,  the  presence  of  occasional 
premature  beats  during  the  periods  of  quiescence  is  extremely 
suggestive  that  the  tachycardia  is  due  to  new  rhythm 
production. 

The  curves  are  illustrated  by  Fig.  35-37.  In  Fig.  35 
the  onset  and  offset  of  the  period  of  tachycardia,  due  to 
abnormal  impulse  formation  at  a  new  auricular  focus,  is 
shown.  The  slow  periods  to  left  and  right  of  it  are  irregular, 
for  premature  contractions  interrupt  them.  The  terminations 
of  two  long  paroxysms  are  shown  in  Fig.  36  and  37.  The 
noteworthy  features  of  such  curves  are  several.  The  changes 
from  the  slow  to  the  fast  and  from  the  fast  to  the  slow 
ventricular  rates  are  quite  abrupt.     Following  each  paroxysm 


Simple  Paroxysmal   Tachycardia.  61 

is  a  relatively  long  pause,  and  this  forms  the  first  of  a  series  of 
pauses  in  a  period  of  retarded  rate.  The  rate  at  the  actual 
termination  is  almost  always  slower  than  the  average  rate 
during  the  periods  of  quiescence  ;    quickening,  which  is  best 


■  i  iw mm 1 1 ii i in 1 1 ii i in" i» mwmn minim niMimm i.inin rwrwwww 


Fig.  35. 


llllllllll        llll       II       II 

Fig.  36. 


^mrwvTnnnryyTrif  rv  * 


^iMaaaA/iAAaaa/iAMaji 


Fig.   37. 

Fig.  35  to  37.  Three  radial  curves,  taken  from  separate  cases  of  paroxysmal 
tachycardia.  In  Fig.  35  a  short  and  complete  paroxysm  is  shown.  In 
Fig.  36  and  37  the  terminations  of  longer  paroxysms  are  seen.  Note  the 
abrupt  onset  and  offsets  of  the  paroxysms,  the  pauses  in  which  they 
terminate,  the  irregularity  of  the  slow  periods  and  the  regularity  of  the- 
fast  periods. 

seen  in  Fig.  36,  occurs  directly  after  the  termination.  The 
slow  rhythm  is  interrupted  by  occasional  premature  con- 
tractions ;  these  may  usually  be  shown,  by  special  methods, 
to  have  the  same  point  of  origin  as  the  paroxysm. 


62  Chapter    V. 

Symptomatology  of  paroxysmal  tachycardia. 

Broadly  speaking,  the  less  frequent  the  attacks,  the  longer 
do  they  last.  In  a  given  patient,  the  duration  of  attacks  is 
fairly  constant,  so  that  the  paroxysms  are  similar  from  time 
to  time.  Paroxysms  of  a  few  seconds  duration  are  not 
uncommon  ;  attacks  which  last  for  several  hours  are  the 
most  frequent  ;  those  of  a  fortnight's  duration  are  rare  ;  the 
attacks  may  be  of  any  intermediate  length.  Paroxysms  of 
accelerated  heart  action  of  longer  duration,  and  of  the  form 
considered  in  the  present  chapter  are  unknown  (see  succeeding 
chapter). 

The  symptoms  accompanying  paroxysms  of  tachycardia 
of  the  kind  considered  are  variable  both  in  their  nature  and  in 
their  degree.  They  are  intimately  dependent  upon  the 
duration  of  the  attack,  the  heart's  rate  during  it,  and  upon  the 
functional  reaction  of  the  heart.  Amongst  those  in  whom 
the  attacks  are  brief,  it  is  not  uncommon  to  find  that  a 
patient  is  entirely  oblivious  to  the  rapid  heart  action  when  it 
occurs,  and  this  is  more  especially  the  case  when  the  subject 
is  elderly  and  of  the  phlegmatic  type  ;  or  he  may  be  conscious 
of  transitory  attacks  only  when  his  attention  is  specifically 
drawn  to  them  or  to  phenomena  commonly  associated  with 
them.  Paroxysms  lasting  half  an  hour  or  longer  are  almost 
invariably  accompanied  by  obvious  symptoms,  and  these 
are  aggravated  as  the  attack  proceeds. 

The  immediate  onset  is  signalled  by  a  sense  of  discomfort 
in  the  region  of  the  heart,  and  this  discomfort  may  amount 
to  slight  or  violent  palpitation.  A  tremor  or  fluttering  in 
the  chest  and  a  beating  in  the  neck  are  common.  General 
effects,  such  as  lassitude,  exhaustion,  coldness  and  sweating 
are  also  amongst  the  early  symptoms.  Later,  flatulence, 
salivation,  nausea  and  vomiting  are  prominent.  These 
alimentary  symptoms  are  common  within  an  hour  or  more  of 
the  onset  and,  once  established,  persist  usually  so  long  as  the 


Simple  Paroxysmal   Tachycardia.  63 

heart  rate  is  maintained.  They  hasten  the  exhaustion  which 
is  common  and  conspicuous  in  attacks  of  long  duration. 
In  many  patients  a  number  of  symptoms  which  are  directly 
referable  to  the  heart  are  added.  These  may  be  divided  into 
two  groups.  First,  anginal  symptoms,  varying  in  intensity 
from  slight  precordial  pain  or  a  sense  of  compression  with  skin 
tenderness,  to  violent  and  continuous  pain,  radiating  in 
the  characteristic  fashion  over  the  chest,  into  the  neck,  into 
the  left  arm  or  both  arms  and  into  the  abdomen.  Wide 
areas  of  hyperalgesia,  corresponding  to  the  distribution  of  the 
lower  cervical  and  upper  thoracic  nerve  roots,  are  frequently 
present  and  persist  after  the  attack  has  ceased  ;  they  are 
accompanied  by  tenderness  of  the  tendons  of  the  sterno- 
mastoids  and  of  the  bellies  of  the  deltoid,  pectoral  and  other 
muscles.  The  patients  complain  of  constriction  of  the  chest, 
variously  described  as  "  a  band  of  tightness,"  "  a  sensation  of 
gripping  "  or  "a  difficulty  in  breathing."  The  second  group 
of  symptoms  is  a  sequel  to  embarrassed  emptying  of  the  heart. 
In  a  number  of  patients,  as  the  attack  proceeds,  the  limits  of 
cardiac  dulness  move  steadily  away  from  the  middle  line, 
and  as  pallor,  which  is  often  an  early  symptom,  becomes  more 
marked,  cyanosis  and  general  venous  engorgement  are  added. 
The  veins  swell  progressively  ;  the  eyes  seem  sunken,  dark 
areas  appear  below  them  and  the  patient  becomes  restless. 
The  liver  bulges  downwards,  its  edge  becomes  palpable  and 
may  pass  the  umbilicus.  Tenderness  is  experienced  when 
the  organ  is  pressed  upon,  and  pulsation  is  felt  in  it  ;  the 
abdominal  muscles  assume  an  increased  rigidity  ;  aching 
pain  develops  in  the  epigastrium  and  right  hypochondrium. 
In  more  exceptional  cases,  puffiness  of  the  ankles  and  face 
develops  after  a  long  continued  attack.  The  spleen  may  also 
show  signs  of  enlargement.  A  cough,  accompanied  by  a  frothy 
and  sometimes  blood-stained  sputum  is  not  infrequent,  and 
signs  of  engorgement  of  the  lungs  in  the  form  of  sibilant  rhonchi 


64  Chapter    V. 

and  moist  rales  are  found  at  the  bases.  Collapse  of  the  patient 
is  prominent  in  the  later  stages.  The  attack  may  terminate 
in  progressive  failure,  delirium,  ascites,  general  anasarca  and 
death.  Unexpected  death  also  ends  the  attack  on  occasion, 
but  the  great  majority  of  the  paroxysms  cease  at  the  abrupt 
resumption  of  the  normal  rhythm.  The  actual  cessation  of 
the  attack  is  marked  by  symptoms  of  its  own,  a  sharp  stabbing 
pain  in  the  chest,  or  one  or  more  forcible  thumps  of  the  heart. 
But  as  a  rule  the  patient  speaks  only  of  relief.  Nothing  is 
more  remarkable  than  the  rapidity  with  which  the  natural 
circulatory  conditions  are  restored,  when  the  abrupt  fall  of 
pulse  rate  comes.  The  dilatation  of  the  heart  and  the 
accompanying  engorgement  of  the  neck  veins  vanish  as  it 
were  by  magic.  The  liver  recedes  beneath  the  ribs,  respiration 
becomes  free,  the  pain  is  subdued  and  the  remaining 
symptoms  subside.  Quantities  of  flatus  and  limpid  urine 
are  often  passed  after  an  attack. 

A  varying  degree  of  exhaustion  follows  the  severe  attack, 
the  cough  may  continue  for  a  few  hours  or  days,  and  skin  and 
muscle  tenderness  commonly  persists  for  some  while. 

Differential  diagnosis. 

The  diagnosis  of  paroxysmal  tachycardia,  during  an 
attack,  rests  upon  careful  attention  to  the  history  of  the 
patient  and  to  those  physical  signs  and  symptoms  which 
have  been  enumerated  already.  As  a  rule  there  is  little 
difficulty.  But  a  number  of  errors  do  occur,  and  the  chief 
of  these  may  be  mentioned  ;  they  mostly  depend  upon  the 
prominence  of  symptoms  which  are  referred  to  other  organs, 
and  consequently  upon  a  hurried  or  neglected  examination 
of  the  organ  at  fault. 

The  stasis  of  the  lungs,  with  dulness  and  crepitations 
at  the  bases,  has  been  attributed  to  pneumonia.  It  is  an 
error  which  should  not  happen,  for  it  is  always  accompanied 
by  signs  of  venous  congestion  in  other  organs.     When  it  has 


Simple  Paroxysmal  Tachycardia.  65 

occurred,  I  believe  it  has  been  largely  attributable  to  under 
estimation  of  the  heart  rate,  and  the  mistake  emphasises 
the  rule  that  the  heart  rate  should  be  taken  from  the  apex 
beat  and  not  from  the  wrist. 

Anginal  pain,  maximal  in  the  abdomen  and  accompanied 
by  abdominal  rigidity,  vomiting  and  signs  of  collapse,  has 
been  mistaken  for  the  symptom  of  a  perforated  gastric  ulcer, 
and  has  led  to  a  dangerous  and  needless  laparotomy  ;  and 
this  in  a  patient  in  whom  cardiac  dilatation,  engorgement  of 
the  veins  and  excessive  heart  acceleration,  were  overlooked 
in  the  absence  of  conspicuous  cyanosis. 

A  large  number  of  cases  are  grouped  under  the  com- 
prehensive term  "  heart  strain,"  and  this  is  applied  especially 
to  the  patient  in  whom  the  first  attack  has  been  hastened  by 
effort. 

More  than  one  instance  has  come  to  my  notice,  in  which 
"  acute  cardiac  dilatation  "  has  sufficed  as  a  diagnosis  in  a 
pregnant  woman,  suffering  in  reality  from  a  rheumatic  heart 
with  mitral  stenosis.  A  rheumatic  history  is  not  uncommon 
in  cases  of  paroxysmal  tachycardia,  and  the  characteristic 
murmurs  of  mitral  stenosis,  when  this  valve  lesion  is  present, 
are  usually  masked  during  the  attack.  A  history  of  rheu- 
matic fever,  or  a  slight  systolic  thrill  and  an  accompanying 
apical  murmur,  may  suggest  a  more  correct  interpretation 
of  the  case. 

The  chief  difficulty  arises,  as  these  instances  illustrate, 
when  a  patient  is  seen  for  the  first  time  in  an  attack,  and  this 
is  especially  so  when  no  clear  history  is  obtainable.  When 
a  regular  heart  rate  exceeds  160  per  minute  in  an  adult,  the 
presence  of  a  new  rhythm,  rather  than  acceleration  of  the 
normal  rhythm,  should  always  come  first  to  mind  ;  it  may  be 
suspected  even  at  lower  rates.  The  reaction  of  the  rate  to 
posture  is  important.  It  is  perfectly  true  that  very  high 
pulse  rates  are  met  with  in  exophthalmic  goitre,  in  pulmonary 


66  Chapter    V. 

tuberculosis,  in  alcoholism  and  other  conditions,  but  the 
presence  or  absence  of  the  diseases  or  intoxication  in  question 
may  usually  be  ascertained  and  the  conditions  differentiated. 
Failing  positive  evidence  from  these  sources,  an  examination 
of  the  heart  rate  in  its  response  to  posture  is  of  service.  In 
the  aforesaid  conditions  a  notable  or  marked  decrease  of  rate 
at  or  shortly  after  the  assumption  of  the  supine  posture  is 
the  rule.  Where  we  deal  with  a  new  rhythm,  posture 
influences  the  rate  inappreciably,  if  at  all,  neither  is  it  affected 
by  repeated  swallowing  or  the  suspension  of  respiration. 
A  persistent  tachycardia  of  140  or  upwards,  maintained  under 
a  variety  of  circumstances,  should  always  suggest  the  presence 
of  a  new  and  extraneous  heart  rhythm. 

Patients  who  are  the  subjects  of  relatively  brief  attacks 
occasionally  seek  advice  during  periods  of  quiescence  on  the 
score  of  attacks  of  faintness,  palpitation,  rapid  heart  action, 
etc..  The  true  nature  of  the  condition  may  be  suspected  or 
proved  by  careful  examination.  The  history  of  the  sensations 
at  onset  or  offset  are  then  most  valuable.  The  complete 
absence  of  symptoms  or  physical  signs  of  cardiac  involvement, 
and  especially  the  absence  of  occasional  or  frequent  premature 
beats,  should  suggest  causes  other  than  those  which  we  are 
considering,  though  they  are  not  finally  excluded  thereby. 
In  a  neurotic  subject,  excessive  force  of  the  cardiac  action  and 
excessive  consciousness  of  the  beat  are  the  most  probable 
explanations.  In  cases  of  doubt  an  effort  should  be  made  to 
investigate  the  heart  during  an  attack.  A  prolonged  exami- 
nation of  the  patient  is  sometimes  rewarded  by  the  discovery 
of  brief  paroxysms  of  true  paroxysmal  tachycardia,  for  the 
patient  so  affected  is  often  the  subject  of  more  attacks  than 
those  of  which  he  is  conscious. 

The  prognosis. 
The   prognosis   of   the   individual   attacks   contains   an 
element    of    uncertainty.        Death    during    paroxysms    has 


Simple  Paroxysmal   Tachycardia.  67 

occurred  on  not  a  few  occasions,  but  the  great  majority  of  the 
paroxysms  are  tolerated.  Several  prognostic  aspects  need 
emphasis.  The  symptoms  of  the  patient  are  largely 
governed  by  the  reaction  of  the  nervous  system  ;  neurotic 
subjects,  especially  women,  awaken  needless  anxiety.  The 
duration  of  the  observed  paroxysm  and  the  length  of  previous 
seizures  have  to  be  considered.  The  outlook  is  more  ominous 
when,  after  a  continuation  of  several  days,  the  heart  shows 
signs  of  progressive  weakening,  manifested  by  steady  increase 
in  its  size  and  by  the  supervention  of  pulmonary  and  hepatic 
congestion.  The  strength  of  the  pulse  is  no  indication  of  the 
future,  it  may  be  scarcely  perceptible  in  repeated  attacks. 
The  gravest  symptoms  are  those  of  increasing  respiratory 
embarrassment,  consequent  upon  oedema  of  the  lungs,  and 
the  onset  of  delirium  and  general  anasarca.  Nevertheless 
it  often  happens  that  when  embarrassment  is  profound  the 
paroxysm  ends,  and  the  patient  passes  in  a  few  minutes  from 
a  condition  of  acute  distress  and  seemingly  the  utmost 
gravity  to  one  of  relative  comfort  and  safety. 

The  prognosis  of  the  malady  as  a  whole  should  be  based 
upon  two  chief  considerations  ;  first  and  most  important, 
upon  an  estimate  of  the  endurance  of  the  cardiac  muscle,  and 
secondly  upon  the  severity  of  the  trials  through  which  it 
passes.  The  estimate  of  the  first  factor  is  formed  from  the 
signs  and  symptoms  between  the  attacks  and  from  the 
reaction  to  moderate  effort.  The  prognosis  in  a  case  of 
paroxysmal  tachycardia  is  the  same  as  that  in  a  similar  case 
which  shows  no  attacks,  but  with  the  following  reservations  : 
the  attacks  are  themselves  important  indications  of  muscle 
damage,  and  the  attacks  frequently  place  the  life  of  the 
patient  in  jeopardy.  The  reaction  of  the  heart  to  the  attacks 
is  also  of  importance.  A  healthy  heart  reacts  to  a  pure 
increase  of  rate,  amounting  to  a  doubling  of  the  normal  rate, 
by  decreasing  in  size,  and  the  circulation  may  be  maintained 

F  2 


68  Chapter    V. 

for  long  periods.  A  diseased  muscle  reacts  by  dilating.  The 
degree  of  dilatation  and  the  rapidity  of  its  onset  and  progress- 
consequently  suggest  the  degree  of  muscular  involvement. 

The  estimate  of  the  second  factor  involves  a  survey  of 
the  length  and  frequency  of  the  attacks  and  the  heart  rate 
during  such  attacks,  as  they  are  summed  up  by  observation 
and  the  previous  history  ;  but  as  the  attacks  may  cease  at 
any  time  never  to  return,  and  as  we  are  ignorant  of  the 
grade  of  injury,  if  such  injury  exists,  which  single  paroxysms 
impose  upon  the  heart,  the  value  of  these  considerations  in 
the  completion  of  the  prognosis  has  its  limitations.  The 
possibility  of  death  in  a  seizure  is  an  uncertain  factor  ;  it 
necessitates  caution  in  prognosis  when  the  paroxysms  are  of 
long  duration. 

The  prognosis,  where  little  further  sign  of  cardiac  muscle 
damage  is  found,  and  where  the  paroxysms  are  infrequent  and 
of  a  few  hours  duration,  and  the  rate  not  very  excessive,  is 
favourable  ;  such  paroxysms  do  not  curtail  life  as  a  rule,  and 
a  prospect  of  long  years  may  be  spoken  of  to  young  subjects 
without  hesitation.  These  patients  always  wish  to  know 
whether  they  will  ever  be  free  from  attacks.  They  may 
be  told  that,  although  such  freedom  cannot  be  promised,  the 
prospect  of  it  is  fair.  The  prognosis  as  a  whole  starts  from 
this  foundation,  and  as  muscle  or  valve  lesions  are  more  in 
evidence,  as  the  attacks  are  longer  and  more  frequent,  as  the 
heart  acceleration  is  greater,  and  as  the  patient  is  older,  so 
the  outlook  is  less  hopeful. 

The  treatment. 

The  treatment  of  paroxysmal  tachycardia  may  be 
conveniently  dealt  with  from  two  standpoints  ;  the  manage- 
ment of  the  attacks  themselves,  and  the  care  of  the  patient 
during  the  general  course  of  the  malady. 


Simple  Paroxysmal  Tachycardia.  69 

Are  we  aware  of  any  remedy  which  will  infallibly  abolish 
a  paroxysm  of  tachycardia  ?  The  answer  to  this  question 
is  in  the  negative.  I  have  frequently  seen  attacks  of  several 
hours  duration  terminate  shortly  after  the  administration 
of  certain  remedies  or  after  certain  interferences.  The  patients 
who  are  the  subjects  of  them  are  often  aware  of  and 
adopt  certain  curative  measures.  In  some  instances  the 
assumption  of  a  given  posture,  sitting  and  placing  the  head 
between  the  knees,  for  example,  or  lying  supine,  is  a  certain 
remedy.  The  induction  of  vomiting,  the  relief  of  flatulence, 
or  the  application  of  a  tight  abdominal  binder  may 
be  immediately  and  constantly  efficacious  in  given  cases. 
I  have  seen  the  application  of  an  icebag  to  the  precordium, 
a  remedy  which  always  affords  relief,  speedily  terminate 
attacks.  Similarly  they  have  ceased  shortly  after  the 
administration  of  a  single  intravenous  injection  of  digitalin 
(1-100  gr.)  or  strophanthin  (1-250  gr.).  Firm  pressure  upon 
one  or  other  vagus  nerve  as  it  lies  in  the  carotid  sheath  has 
been  successful.  But  much  more  often  than  not,  such 
remedies  are  without  effect  and  the  treatment  finally  adopted 
becomes  palliative  or  symptomatic.  Rest  is  enjoined,  and 
attention  is  paid  to  the  wishes  of  the  patient  in  respect  of 
posture.  Most  frequently  these  unfortunate  people  prefer 
to  lie  well  propped  with  pillows  ;  sometimes  they  prefer  to 
stand.  The  dietary  should  be  fluid,  bland  and  as  restricted 
as  possible.  Iced  water  or  milk  are  well  borne  and  are  often 
beneficial. 

Local  applications,  the  icebag,  a  mustard  plaster, 
leeches  or  cupping  over  a  distended  or  pain-giving  organ, 
be  it  the  heart  or  the  liver,  often  afford  great  relief.  Pain,  if 
general,  may  be  combated  by  more  general  remedies,  such  as 
chloral  or  morphia  ;  but  these  drugs  are  not  often  called  for. 
The  induction  of  sleep  in  long  continued  paroxysms  is 
essential,  and  fortunately  chloral  and  the  opiates  may  be 


70  Chapter   V. 

employed  with  safety.  Serious  engorgement  of  the  heart 
and  signs  of  progressive  lung  oedema  or  grave  venous  stasis 
are  indications  for  venesection.  The  letting  of  8  or  12  oz. 
of  blood  will  be  followed  by  improvement  ;  but  the  occasion 
does  not  often  arise.  Respirator}7  embarrassment  is  relieved 
and  sleep  induced  by  the  administration  of  oxygen  ;  this 
gas  is  best  given  through  a  tight  fitting  mask  which  covers 
the  whole  face,  so  that  high  percentages  are  breathed. 

The  treatment  of  the  malady  as  a  whole  is  largely 
governed  by  the  condition  of  the  heart  between  the  attacks. 
A  searching  inquiry  may  reveal  exciting  causes  of  paroxysms  ; 
often,  sudden  exertion  or  emotion  is  the  chief  provocative, 
so  that  the  cessation  of  employment  becomes,  not  infrequently, 
imperative.  General  care  of  the  health,  the  cleanliness  of  the 
mouth  and  throat,  the  orderliness  of  the  dietary  and  the 
remedying  of  dyspeptic  troubles  and  constipation  may  ward 
off  the  crises.  The  continued  wearing  of  an  abdominal 
belt,  applied  before  rising  and  discarded  at  bedtime  is 
sometimes  accompanied  by  the  happiest  of  results. 

Where  other  remedies  fail,  a  full  course  of  digitalis*  may 
ultimately  improve  the   condition. 

The  paroxysms  themselves  do  not  contra-indicate 
the  careful  administration  of  general  anaesthetics,  should 
they  be  necessary. 


*  By  a  full  course,  I  wish  to  denote  a  course  of  the  drug  which  will 
produce  a  definite  reaction  in  the  form  of  nausea  or  headache,  and  the  subse- 
quent administration  of  the  drug  for  several  weeks,  in  doses  which  are  tolerated. 
As  a  rule  3ss"3i  °f tne  tincture  or  §ss-^i  of  the  fresh  infusion  may  be  given  daily 
for  the  first  week,  the  dose  being  increased  until  symptoms  appear,  and  finally 
reduced  to  the  maximal  quantity  tolerated  without  undue  discomfort.  Small 
doses  of  digitalis  and  the  allied  drugs  are  without  appreciable  effect.  Aconite, 
strychnine,  belladonna  and  its  allies  should  be  avoided. 


(     71     ) 


Chapter  VI. 


AURICULAR    FLUTTER. 


Definition. 


Auricular  flutter  may  be  arbitrarily  defined  as  a  condition 
in  which  the  normal  beats  of  the  auricle  are  submerged  by 
contractions  of  this  chamber  in  response  to  a  series  of  new, 
rhythmic  and  pathological  impulses,  varying  in  rate  from 
200  to  350  per  minute. 

The  nature  of  the  flutter. 

A  strict  separation  of  auricular  flutter  from  simple 
paroxysmal  tachycardia,  the  disorder  described  in  the 
preceding  chapter,  is  not  at  present  possible  ;  yet  the 
symptomatology,  course  and  treatment  of  new  auricular 
rhythms  of  extreme  rate,  are  sufficiently  special  that  for 
descriptive  purposes  it  is  convenient  to  retain  them  in  a 
separate  category.  Although  it  may  be  perfectly  true  that  an 
acceleration  of  the  auricle  to  210  per  minute  does  not  provoke 
widely  different  symptoms  from  an  acceleration  at  190  per 
minute,  yet  between  the  features  of  tachycardia  at  190  and 
300  per  minute  there  is  as  a  rule  little  resemblance.  Extreme 
acceleration  of  the  auricle  has  its  special  characters,  and  the 
arbitrary  line  of  separation  is  drawn  at  200  per  minute, 
because  these  special  characters  begin  to  appear  when  the 


72  Chapter  VI. 

rate  is  so  far  enhanced.  Perhaps  the  most  notable  feature  of 
flutter,  or  extreme  acceleration  of  the  auricle,  is  its  almost 
invariable  association  with  heart-block.  Flutter,  so  far  as 
we  know,  arises  in  the  auricle  only,*  and  the  rate  of  the 
auricular  contractions  is  so  great,  that  the  ventricle  can  rarely 
keep  the  pace.  The  usual  auricular  rates  are  from  260  to 
320  per  minute  ;  the  systoles  of  the  auricle  follow  each  other 
so  rapidly  that  the  diastoles  are  reduced  almost  to  vanishing 
point .f  The  usual  ventricular  rates  are  from  130  to  160, 
exactly  half  the  auricular  ;  for  2  :  1  heart-block  is  generally 
present  when  the  patient  first  comes  under  observation 
(Fig.  38).     The  new  impulses  which  drive  the  auricles  in  this 


llllllllllllll 

leiiiiiiiini 


Fig.  38.  A  diagrammatic  representation  of  auricular  flutter.  The  abnormal 
auricular  beats  are  broken  in  their  centres.  The  auricular  rate  is  very 
rapid  ;  the  ventricular  rate  is  also  rapid,  but  is  half  the  auricular.  2  :  1 
heart-block  is  present. 


merciless  fashion  probably  spring  from  a  single  focus  in  the 
auricular  tissue,  and  as  in  the  simple  form  of  paroxysmal 
tachycardia,  this  focus  is  probably  an  unnatural  one.  The 
mischief  lies  at  a  distance  from  the  pacemaker,  and  the  reins 
of  control,  the  inhibitory  nerves,  are  powerless.  The  auricle  has 
veritably  seized  the  bit  with  its  teeth.    The  ventricle,  shielded 


*  Ventricular   flutter   is   unknown   clinically  ;     it   is  probably   unknown 
because,  continuing,  it  would  inevitably  kill  the  subject  of  it. 

t  These  facts  have  been  elucidated  electrocardiographically. 


Auricular  Flutter.  73 

from  the  whip  by  the  auriculo-ventricular  bundle,  lags 
behind.  2  :  1  heart-block  is  the  rule  ;  but  any  grade  of  block 
may  be  present.  Thus  it  happens  that  while  the  auricle 
races  at  300  per  minute,  the  ventricle  may  beat  at  150 
(2  :  1, heart-block)  ;  at  75  (4  :  1),  a  normal  rate,  or  at  30  to  38 
(complete  dissociation).  The  speed  of  the  auricle  once  set  is 
wonderfully  uniform  ;  it  may  vary  but  a  few  beats  per  minute 
over  long  periods  of  time  ;  its  beating  is  always  regular.  The 
responses  of  the  ventricle  are  often  regular  ;  but  may  also  be 
irregular,  when  the  impulses  from  the  auricle  are  chosen  at 
irregular  intervals  ;  especially  is  this  the  condition  when  one 
uniform  grade-  of  heart-block  is  passing  into  another.  But 
■even  when  the  ventricle  beats  irregularly,  as  each  of  its 
responses  is  to  an  auricular  contraction  forming  one  of  a 
perfectly  regular  series,  the  ventricular  contractions  lie  in  the 
■curves  at  definite  points  (Fig.  39),  which  may  be  prejudged 


IIIIIIIIIIIIIIIIIIIIIIIIII 

milium  imiiiiiiiim 

Wnrnii 

Fig.  39.  A  similar  representation  of  auricular  nutter  with  irregular  response 
of  the  ventricle.  The  irregularity  is  of  such  a  kind  that  the  beats  of  the 
ventricle  come  in  groups  which  are  accurately  repeated  from  time  to 
time.      Note  the  change  in  the  As-Vs  interval,  and  compare  with  Fig.  11. 

accurately  if  the  grade  of  block  is  known.  The  point  at 
which  a  ventricular  beat  is  placed  is  governed  by  laws 
described  under  heart-block  in  Chapter  III. 

Attacks  of  flutter  are  on  exceptional  occasions  of  quite 
brief  duration  ;    usually  they  last  for  months  or  years. 


74  Chapter  VI. 

Etiological  and  pathological  relations. 

Age.  Flutter  is  a  comparatively  rare  condition,  and  is 
usually  associated  with  advanced  years.  In  a  series  of  27 
collected  cases  the  age  incidence  is  as  follows  : — 

Age  20-30   30-40   40-50   50-60   60-70   70-80 

Cases  of  my  own  series  .  .  1  1  2  3  8  2 

Remaining  cases   ....  1  3  1  2  2  1 


2  4  3  5         10  3 

Sex.     Of  this  series  22  were  males  and  only  5  females. 

Relations  to  infective  disease,  etc..  As  a  general  rule,  no- 
previous  infection  can  be  traced.  Rheumatic  fever  or 
syphilis  has  seemed  responsible  in  some  cases,  and  in  others 
there  has  been  an  antecedent  infection  of  the  urinary  tract 
or  history  of  recurrent  attacks  of  gout. 

Associated  conditions.  Occurring  as  it  does  in  elderly 
cases,  flutter  is  often  associated  with  arterial  sclerosis  ; 
much  increase  of  the  heart's  dulness  is  uncommon  ;  as  a  rule 
there  are  no  murmurs,  but  any  of  the  valve  lesions  may  be 
discovered.  There  are  nearly  always  some  signs  of  degenera- 
tion of  the  heart  muscle,  as  witnessed  to  by  the  symptoms 
of  the  patient,  when  the  heart  beats  at  normal  rates. 

Of  the  morbid  anatomy,  we  have  little  or  no  knowledge. 

The  recognition  of  flutter. 

In  a  number  of  patients,  the  presence  of  auricular 
flutter  may  be  recognised  by  ordinary  clinical  means  ;  but  in 
perhaps  a  larger  number,  the  diagnosis  is  only  possible  when 
special  methods  (the  electrocardiographic  particularly)  are 
employed. 

During  the  2  :  1  heart-block  phase.  When  flutter  patients 
are  first  seen,  the  rate  of  the  ventricular  action  is  usually 
half  the  auricular.     The  history  often  includes  palpitation,  of 


Auricular  Flutter.  75 

sudden  onset  months  or  years  previously.  A  regular  and 
persistent  ventricular  action  of  from  130-160  per  minute  in  an 
elderly  subject  is  a  most  suspicious  circumstance,  and  its 
discovery  should  always  be  followed  by  a  special  examination 
for  other  signs  of  flutter.  The  patient  may  give  a  history  of 
short  paroxysms  of  many  years  standing  and  may  speak  of 
this  the  final  attack  which  he  is  unable  to  discard.  If 
tachycardia  persists  for  a  month  or  more  at  one  of  the  stated 
rates,  and  there  is  absolutely  no  change  of  rate  with  change 
of  posture,  rest  or  exercise,  the  condition  is  almost  certainly 
flutter.  A  most  suggestive  incident  is  the  constant  repetition 
of  the  same  high  pulse  reading  in  the  pulse  chart,  or  the  finding 
of  exactly  the  same  high  pulse  rate  at  intervals  of  weeks  or 
months. 

From  time  to  time  in  certain  individuals,  and  usually 
during  periods  of  emotion  or  exertion,  the  ventricular  rate 
springs  momentarily  to  the  full  auricular  rate  ;  the  resulting 
disturbance  is  profound,  and  patients  who  retain  consciousness 
subsequently  give  vivid  accounts  of  the  experience  ;  fainting 
is  common  in  flutter  patients. 

Firm  pressure  upon  the  carotid  sheath,  on  left  or  right 
side,  sufficient  to  obliterate  the  vessel  and  stimulate  the  vagus 
nerve,  always  produces  a  conspicuous  slowing  of  the  pulse  or 
lapse  of  many  beats  (Fig.  40).  Similarly,  digitalis,  given  in  full 
doses,  always  slows  the  pulse  and  creates  irregularity.  The 
radial  curves,  when  the  pulse  is  fast,  often  exhibit  alternation 
(see  Chapter  VIII). 

During  the  stage  of  irregular  responses.  If  the  responses 
of  ventricle  are  irregular,  a  little  exercise,  often  no  more  than 
raising  a  limb  from  bed,  immediately  accelerates  the 
ventricular  action  and  induces  perfect  regularity  of  the  pulse 
(2:1  heart-block)  and  this  regular  pulse  action  may  then  be 
tested  in  the  manner  described  in  the  preceding  paragraphs 
(Fig.  41). 


76 


Chapter  VI. 


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Auricular  Flutter. 


77 


The  character  of  the  radial  curves  gives  an  immediate 
clue  to  the  condition  (Fig.  42a  and  explanation). 


Fig.  42a.  A  series  of  three  radial  curves  from  a  case  of  nutter,  showing  the 
chief  features  of  the  irregularities  produced  by  mixed  responses.  The 
curves  have  a  superficial  resemblance  to  premature  contractions  ;  but 
that  the  irregularity  is  not  produced  in  this  fashion  is  clearly  indicated 
by  the  manner  in  which  the  curves  "  space."  The  bracketed  portions 
of  each  curve  are  of  equal  duration,  and  they  are  of  equal  duration  because 
they  correspond  to  equal  numbers  of  auricular  beats.  The  number  of 
auricular  contractions  to  each  ventricular  cycle  is  marked  above  each 
pulse  beat. 

When  the  responses  of  the  ventricle  are  infrequent.  It  is 
under  these  circumstances  that  flutter  is  so  difficult  to 
recognise  by  ordinary  clinical  means.  A  patient  may  possess 
a  fluttering  auricle  and  the  pulse  may  be  within  normal 
limits  of  rate  and  may  be  regular.  Fortunately  such  cases 
are  rare  ;  moreover,  the  failure  to  detect  the  flutter  at  such 
times  is  relatively  of  less  consequence.  In  some  patients  the 
vibratory  movements  of  the  auricle  are  transmitted  to  the 
veins  of  the  neck  and  may  be  identified  (Fig.  426). 

The  symptomatology  of  flutter. 
The  symptoms  associated  with  auricular  flutter  need  not 
long  detain  us.  In  patients  in  whom  the  acceleration  occurs 
in  short  paroxysms  the  symptoms  are  identical  with  those 
of  simple  paroxysmal  tachycardia  ;  they  vary  in  intensity 
according  to  the  heart  rate  and  according  to  the  resisting 
power  of  the  ventricular  muscle. 


78 


Chapter   VI. 


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Auricular  Flutter. 


79 


But  in  patients  who  experience  longer  periods  of  disturbed 
heart  action,  and  these  are  more  frequent  for  nutter  generally 
persists  for  months  or  years,  the  subjective  sensations  are 
modified.  Although  the  reason  is  not  clear,  the  symptoms  of 
flutter  seem  less  profound  than  is  to  be  expected  from  a  study 


vjvM^VJ 


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Fig.  43.  A  series  of  four  curves,  showing  the  effect  of  digitalis  medication 
upon  nutter,  (a)  The  heart  is  beginning  to  respond  to  digitalis  and 
occasional  periods  of  4  :  1  heart-block  are  seen,  interrupting  an  otherwise 
regular  2  :  1  mechanism  ;  the  rate  of  the  auricles  was  264  per  minute,  and 
that  of  the  ventricles  132.  (b)  Further  slowing  a  few  days  later.  The 
beats  of  the  ventricle  now  occur  in  groups,  or  the  mechanism  is  reduced 
to  4  :  1  grade  of  heart-block,  (c)  A  few  days  later  ;  the  ventricle  becomes 
grossly  irregular  as  the  result  of  the  establishment  of  fibrillation.  The' 
digitalis  having  been  withdrawn,  the  normal  and  regular  mechanism  is 
resumed  (d)  ;    the  rate  of  the  auricle  and  ventricle  being  64  per  minute. 

of  many  more  simple  crises  of  tachycardia.  Thus,  not 
infrequently,  the  action  of  the  heart  may  be  accelerated  to 
130  or  150  for  periods  of  a  year  or  more,  and  yet  the  symptoms 
consist  of  little  more  than  a  sense  of  exhaustion  and  fatigue 
after  slight  exertion.  The  occupations  of  such  patients  are 
limited,  but  signs  of  failure  in  the  form  of  stasis  and  dropsy 


80  Chapter  VI. 

may  not  occur.  Such  tolerance  is  to  be  attributed  perhaps 
to  relatively  powerful  ventricular  muscle.  Naturally  there 
are  cases  of  nutter  in  which  signs  of  congestion  are  visible 
at  an  early  stage  ;  but  in  reviewing  a  series  of  cases,  one 
cannot  but  be  impressed  by  the  infrequence  of  these  signs 
of  failure,  as  compared  to  their  incidence  in  other  tachycardias 
giving  similar  ventricular  rates. 

As  I  have  already  indicated,  there  is  an  additional 
symptom  complex  in  nutter  ;  it  results  when  the  ventricle 
assumes  the  full  auricular  rate  ;  an  acceleration  of  the 
ventricle  to  300  per  minute  places  the  life  of  the  subject  in 
immediate  jeopardy,  the  symptoms  are  profound,  and 
consciousness  is  usually  lost  ;  such  attacks,  being  survived, 
are  necessarily  fleeting. 

The  prognosis. 

The  time  has  not  arrived  when  we  may  speak  of  the 
prognosis  in  auricular  flutter  from  long  experience  of  the 
cases  ;  the  malady  is  but  newly  discovered.  I  have  known 
the  condition  to  last  for  four  years,  the  ventricle  beating 
without  cessation  at  160  per  minute.  How  much  longer 
this  high  rate  may  be  maintained  in  the  presence  of  a  tolerably 
efficient  circulation,  we  cannot  say.  Of  my  17  cases,  one 
only  has  succumbed,  and  this  as  an  immediate  sequel  to 
prostatectomy  ;  but  as  yet  most  of  the  patients  have  been 
under  observation  only  for  short  periods  of  time. 

We  may  gather  a  general  idea  of  the  prospect  upon  the 
lines  discussed  in  treating  of  the  simple  paroxysms  of  the  last 
chapter.  It  should  be  based  upon  a  general  consideration  of 
the  strength  of  the  heart  muscle,  and  of  the  burden  which 
this  muscle  has  to  carry.  Important  in  this  respect  is  the 
response  to  treatment,  for  most  cases  are  amenable  to 
specific  measures,  as  we  shall  see  in  the  succeeding  paragraphs. 


Auricular  Flutter.  81 

The  treatment. 

The  treatment  of  long  continued  flutter  of  the  auricles  is 
often  conspicuously  successful.  Even  after  the  acceleration 
has  lasted  for  many  months  or  even  several  years  the  natural 
rhythm  of  the  heart  may  be  restored  by  suitable  medication. 
The  remedy  is  digitalis  or  an  allied  drug.  My  experience 
tells  me  that  the  ventricular  rate  can  always  be  reduced  by 
giving  digitalis  or  strophanthus  in  full  doses,  and  may  be 
maintained  at  the  reduced  rate  so  long  as  treatment  is  continued . 

Further,  I  have  found,  that  if,  having  obtained  this 
reaction,  the  dosage  can  be  increased,  the  flutter  ceases  and 
fibrillation  (a  condition  described  in  the  next  chapter)  takes 
its  place  ;  if  now  the  remedy  is  withdrawn,  the  fibrillation 
vanishes  in  most  cases  and  the  normal  rhythm  is  immediately 
resumed.  I  have  seen  these  changes  in  a  number  of  patients 
and  can  speak  confidently  of  the  success  of  the  remedy. 
Occasional  intolerance  to  the  drug,  the  onset  of  gastro- 
intestinal symptoms,  appears  to  be  the  sole  limitation  ; 
strophanthin  may  then  be  administered  intravenously  with 
equally  happy,  and  much  more  speedy,  results.  It  may  be 
asked  if  the  flutter  ever  returns  when  it  has  been  abolished  ? 
In  one  of  my  cases  it  has  returned,  but  renewed  treatment 
again  restored  the  normal  rhythm  and  this  has  since  persisted. 
The  secret  of  the  treatment  seems  to  lie  in  the  rupture 
of  a  vicious  circle.  Flutter,  once  it  comes,  promotes  and 
establishes  itself  ;  the  same  tendency  is  found  in  fibrillation, 
a  condition  which  we  shall  discuss  presently.  Being  checked, 
the  cause  of  its  persistence  seems  to  be  removed. 

When,  in  such  patients  as  have  signs  of  cardiac  failure, 
flutter  is  removed  and  the  normal  rhythm,  with  normal  heart 
rate,  takes  its  place,  the  change  in  the  general  condition  is 
remarkable  and  almost  immediate.  Engorgement  and  dropsy 
rapidly  disappear  ;  breathlessness  and  other  discomforts  are 
relieved ;  the  customary  occupations  of  life  may  be  resumed. 


(     82 


Chapter  VII. 


AURICULAR    FIBRILLATION. 

Definition. 

A  condition  in  which  normal  impulse  formation  in  the 
auricle  is  replaced  by  stimulus  production  at  multiple 
auricular  foci.  Co-ordinate  contraction  in  the  auricle  is  lost ; 
the  normal  and  regular  impulses  transmitted  to  the  ventricle 
are  absent,  while  rapid  and  haphazard  impulses  produced 
in  the  auricle  take  their  place  and  produce  gross  irregularity 
of  the  ventricular  action. 

The  nature  of  auricular  fibrillation. 

When  we  inspect  the  normally  beating  heart  of  an 
animal,  the  systoles  of  both  auricle  and  ventricle  are  readily 
discerned.  The  movement  of  the  auricle  is  a  sharp  flick, 
most  clearly  perceptible  in  the  length  of  the  auricular 
appendix,  for  in  this  line  the  shortening  is  greatest.  When 
the  auricle  is  forced  into  fibrillation  or  delirium,  the 
appearances  are  quite  distinctive  ;  the  muscular  walls  are 
maintained  in  a  position  of  diastole  ;  systole,  either  complete 
or  partial,  is  never  accomplished  ;  the  structure  as  a  whole 
rests  immobile  ;  but  close  observation  of  the  muscle  surface 
reveals  its  extreme  and  incessant  activity,  rapid  and  minute 
twitchings  and  undulatory  movements  are  visible  over  the 
whole.  It  is  believed  that  the  tissue  mass  has  suffered 
functional  fragmentation  and  that  a  number  of  small  areas 


Auricular  Fibrillation.  83 

give  independent  birth  to  new  impulses.  Further  it  is  held 
that  these  fresh  impulses  are  pathological,  being  similar  to, 
or  identical  with,  those  which  evoke  single  premature  con- 
tractions. The  effect  of  the  auricular  confusion  upon  the 
ventricle  is  twofold.  The  normal,  regular  and  co-ordinate 
contractions  in  the  auricle  are  in  abeyance  and  consequently 
the  ventricle  is  robbed  of  the  regular  impulses  which  form 
its  accustomed  supply.  These  are  replaced  by  numerous 
and  haphazard  impulses,  escaping  to  the  ventricle  from  the 
turmoil  which  prevails  in  the  upper  chamber  ;  the  change  in 
the  action  of  the  ventricle,  when  the  auricle  fibrillates,  is 
consequently  profound.     Its  rate  of  beating  rises  considerably 


II  III  III 


I  I 


Fig.  44.  A  diagrammatic  representation  of  auricular  fibrillation.  The  fibres 
of  the  auricles  do  not  contract  co-ordinately  or  together,  but  the  tissue 
is  broken  up  into  a  number  of  independently  active  areas.  Occasional 
impulses  leave  the  auricle  at  quite  irregular  intervals  and  stimulate  the 
ventricle,  producing  in  it  a  rapid  and  irregular  action. 

and  the  contractions  follow  each  other  in  a  completely 
irregular  fashion.*  This  mechanism  is  diagrammatically 
represented  in  Fig.  44,  in  which  I  have  attempted  to  emphasise 
the  absence  of  co-ordinate  auricular  beats,  the  presence  of 
constant  fibrillary  contraction,  and  the  irregular  responses 
of  the  quickened  ventricle  to  the  new  auricular  impulses. 

Such  are  the  events  in  experiment,  and  those  of  the 
clinical  condition  are  identical,  with  one  proviso  ;   since  in  the 

*  Ventricular  fibrillation  is  incompatible  with  life.  It  is  probably 
responsible  for  many  instances  of  unexpected  death ;  this  end  is  moro 
especially  suspected  in  certain  cases  of  auricular  fibrillation  and  in  death  under 
chloroform  anaesthesia. 

G  2 


84  Chapter  VII. 

experimental  heart  the  tissues  controlling  the  conduction  of 
impulses  are  healthy,  the  rate  of  the  ventricular  contractions 
is  doubled  or  even  trebled  ;  but  in  the  human  subject,  the 
conducting  tissues  may  be  either  intact  or  damaged,  con- 
sequently the  ventricular  rate  varies  widely  in  different 
patients,  according  as  access  to  the  ventricle  is  full  or  limited. 
While  a  free  passage  yields  rates  approaching  200  per  minute, 
damage  to  the  junctional  tissues  may  reduce  the  rate  to  40  or 
less  :    the  usual  rates  lie  between  90  and  140. 

Etiological  and  pathological  relations. 

Age.  The  observed  age  limits  of  fibrillation  are  5  to  84; 
it  is  extremely  rare  before  the  age  of  17  years.  In  studying  the 
age  distribution,  the  cases  are  conveniently  divided  into 
rheumatic  and  non-rheumatic  groups.  This  division  clearly 
shows  that,  independent  of  rheumatism,  the  affection  is 
related  to  advancing  years  ;  as  with  premature  contractions, 
the  highest  incidence  is  in  the  sixth  and  seventh  decade. 
In  the  rheumatic  group,  the  incidence  is  heaviest  between  the 
twentieth  and  thirtieth  years  ;  it  is  almost  as  heavy  in  the 
fourth  and  fifth  decade,  but  lightens  as  the  years  mount 
further. 

Age  distribution  of  auricular  fibrillation  in  141  cases. 

Age  0-10    10-20   20-30   30-40   40-50   50-60   60-70     70-80     80-90    90-100 

Rheumatic 

group       0         4         26         21         23         10  5  0  2 

Non- 
rheumaticO         0  0  2  6  17  18  4  3 

0         4         26         23         29         27         23  4  5 

Sex.  Auricular  fibrillation  is  much  more  common  in 
men  than  in  women,  and  the  preponderance  in  males  is 
chiefly  in  the  non-rheumatic  group.  Where  there  is  a 
rheumatic  history,  the  sexes  bear  the  burden  more  equally. 
The  relative  frequency  of  rheumatic  fibrillation  in  women 
is  linked  with  the  prevalence  of  mitral  disease  in  this  sex  ; 


Auricular  Fibrillation.  85 

mitral  stenosis  and  auricular  fibrillation  are  bosom  com- 
panions. Among  189  subjects  the  sex  distribution  was  as 
follows  : — 


Male. 

Female, 

Rheumatic 

53 

4:1 

Non  -rheumatic   .  . 

44 

13 

Not  noted 

17 

15 

114  75 

Relation  to  infections  ;  associated  conditions.  Amongst 
152  cases,  a  rheumatic  or  choreic  history  has  been  found 
71  times  ;  in  four  instances  at  least,  there  was  a  history  of 
one  or  other  affection  in  the  family.  Amongst  the  remainder, 
mitral  stenosis  was  present  in  26,  and  pericardial  adhesions 
or  effusion  in  two  cases.  If  these  patients  are  collected  to 
form  a  rheumatic  group,  the  subdivision  includes  101  cases,  or 
66  per  cent..  The  prevalence  of  fibrillation  amongst  those  who 
suffer  from  mitral  constriction  is  especially  noteworthy  ;  79 
of  the  cases,  or  52  per  cent.,  had  this  valve  lesion.  The 
relation  to  mitral  stenosis  may  be  traced  in  another  and 
equally  emphatic  manner.  Of  106  cases  of  mitral  stenosis 
collected  in  an  out-patient  department,  22,  or  approximately 
one-fifth,  showed  auricular  fibrillation.  The  proportion 
amongst  in-patients  is  much  higher  ;  it  exceeds  50  per  cent.. 
In  the  table,  I  have  classed  a  group  as  myocardial 
degeneration  ;  it  includes  those  in  whom  the  heart  irregularity 
was  the  outstanding  feature,  though  many  of  the  cases  gave 
signs  of  cardiac  failure  in  addition  to  the  irregularity. 
Aortic  disease,  arterial  disease  and  granular  kidney  are 
the  most  prominent  lesions  in  other  groups.  Of  all 
cases  of  cardiac  failure  admitted  to  a  general  hospital  60 
to  70  per  cent,  manifest  this  disorder  of  the  cardiac 
mechanism  ;  it  is  difficult,  therefore,  to  over-emphasise  its 
importance. 


8G 


Chapter    VII. 


1 

Mitral  stenosis 

51 

Rheumatic  or 

Myocardial  degeneration 

ii 

choreic  history   1 

Pericardial  adhesions 

1 

(n 

1 

Aortic  disease 

6 

k  Renal  diseases 

2 

Rheumatism  or      J  Mitral  stenosis 

2 

1 

1    4 

chorea  in  family  ^Myocardial  degeneration 

2 

'Mitral  stenosis 

19 

Arterial  disease 

7 

Myocardial  degeneration 

17 

Renal  disease 

11 

Aortic  disease 

3 

Aneurism 

2 

No  history  of 

Emphysema  &  bronchitis 

2 

rheumatism  or    i 

Strepto.  endocarditis 

2 

170 

chorea 

Pericardial  adhesions  and 

pericardial  effusion 
Tuberculous  pleurisy 
Syphilitic  heart 
Congenital  heart 
Chronic  alcoholism 
^Pneumonia 

2 

1 
1 
1 
1 

1 

Rheumatism  or 

Mitral  stenosis 

7 

7 

chorea  not  noted 

79 

30 

13 

9 

7 

3 

11 

152 

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Of  etiological  factors,  rheumatism  is  predominant,  as  we 
have  seen  ;  a  history  of  other  infections,  "  influenza  " 
amongst  them,  is  given  by  many  patients,  but  the  influence 
of  these  infections  is  imperfectly  understood. 


*  The  heavy  figures  mark  the  rheumatic  group. 


Auricular   Fibrillation.  87 

Morbid  anatomy.  That  valve  lesions  are  present  in  a 
number  of  the  cases  is  obvious  from  the  bedside  examinations  ; 
enlargement  of  the  whole  heart  is  common,  and  dilatation 
or  hypertrophy  of  the  auricles  is  more  frequent  than  the 
valve  lesions  which  might  be  held  to  account  for  them.  The 
most  constant  structural  alterations,  which  are  found,  are 
discovered  by  histological  examination  of  the  heart  muscu- 
lature. Usually  it  shows  a  more  or  less  intense  grade  of 
subacute  or  chronic  inflammatory  change  progressing  to 
fibrosis,  and  the  auricles  are  conspicuously  affected.  A 
diffuse  fibrosis,  accompanied  by  leucocytic  infiltration  and 
atrophy  of  the  neighbouring  muscle  cells,  is  the  most 
frequent  change. 

Such  is  the  tale  told  by  the  microscope,  but  it  does  not 
justify  us  in  holding  that  the  inflammatory  reaction  is  the 
cause  of  the  altered  mechanism.  We  examine  the  hearts 
of  those  who  die,  and  most  die  with  all  the  classical  signs  of 
heart  failure.  Many  of  the  microscopic  lesions  are  to  be 
regarded  as  the  result  of  infections  producing  heart  failure 
rather  than  fibrillation.  Similar  lesions  are  found  where 
fibrillation  has  never  occurred  ;  and  hearts  which  have  shown 
this  disorder  may  not  present  the  lesions  described. 
The  recognition  of  auricular  fibrillation. 

Auricular  fibrillation  gives  rise  in  a  clinical  case  to  two 
series  of  phenomena  ;  the  one  dependent  upon  the  virtual 
paralysis  of  the  auricle  ;  the  other  dependent  upon  the 
irregularity  of  the  ventricle. 

It  will  be  convenient  to  study  the  ventricular  signs 
first.  The  irregularity  is  most  varied  in  form  according  to 
the  rate  of  the  contractions.  When  the  heart  is  beating 
rapidly  at  100-160  per  minute,  the  grade  of  disorder  is 
maximal.  The  radial  artery  supplies  indifferent  news  of  the 
ventricular  rate,  many  pulsations  fail  to  reach  it  (such  beats 
are  marked  with  asterisks  in  Fig.  46).     The  pulse  is  a  medley 


88 


Chapter    VII. 


A uricular  Fib r illation. 


89 


or 


h  o 


to 


90  Chapter    VII. 

of  beats  of  many  sizes  (Fig.  45),  an  intimate  mingling  of 
changing  pauses  ;  now  the  beats  are  almost  uniform  in 
strength  and  spacing  ;  now  feeble  pulsations  chase  along 
rapidly  ;  now  the  pulse  is  lost  ;  now  it  returns  with  increased 
vigour.  Feel  the  pulse  and  the  mechanism  is  apparent  ; 
the  more  the  disorder,  the  more  certain  the  evidence.  It  is 
when  the  rate  is  slow  that  close  attention  and  more  experience 
are  often  asked  for  with  slower  rate,  the  disorder  is  less 
pronounced  ;  all  the  heart  beats  now  reach  the  wrist  and  the 
irregularity  comprises  minor  variations  in  the  length  of 
pause  (as  in  Fig.  48)  ;  in  such  instances  it  escapes  notice,  and 
a  heedful  examination,  concentrated  upon  its  presence  or 
absence,  alone  brings  it  to  discovery.  Short  pulse  curves 
reveal  the  irregularity  on  all  but  rare  occasions.  The  nature 
of  the  arrhythmia  is  such  that  the  heart  action  is  never  quite 
regular,  and  seldom  do  two  beats  of  a  precisely  equal  character 
or  length  lie  adjacent.  No  two  whole  strips  of  curve  are 
similar  ;  the  pauses  betwixt  beats  bear  no  simple  length 
relation  one  to  another.  Proportion  between  the  force  of 
an  arterial  pulse  and  the  pause  preceding  it  is  often  lost 
(Fig.  45  and  46)  ;  a  strong  beat  succeeds  a  brief  pause  and  a 
weak  beat  succeeds  a  long  one.  When  the  pulse  is  slow,  only 
beat  to  beat  measurement  may  disclose  the  irregularity. 

The  fully  developed  disorder  of  the  ventricle  is  readily 
appreciated  at  the  apex.  The  heart  sounds  are  modified  ; 
they  vary  in  intensity  and  the  variation  runs  hand  in  hand 
with  the  strength  of  the  beats.  First  and  second  sounds  are 
present  with  each  cycle  which  gives  arterial  pulsation  (Fig. 
45)  ;  a  first  sound  stands  isolated  when  the  pulse  beat  is 
missing  (Fig.  46).  If  a  systolic  mitral  murmur  is  present,  it 
accompanies  each  ventricular  contraction  (Fig.  49),  except 
where  the  rate  is  fast,  for  here  it  is  apt  to  vanish.  Aortic 
murmurs  obey  the  general  rule,  their  presence  or  absence  is 
controlled  by  the  efficiency  of  the  respective  beasts  (Fig.  47). 


Auricular  Fibrillation.  91 

The  inactivity  of  the  auricle  is  responsible  for  special 
alterations  of  the  heart  sounds  in  patients  who  have  stenosis 
of  the  mitral  orifice.  It  is  customary  to  allude  to  disappear- 
ance of  presystolic  murmurs  when  the  auricle  fibrillates,  but 
this  statement  is  not  exact.  The  change  in  the  characters  of  the 
murmurs  at  the  onset  of  fibrillation  is  oftentimes  impressive, 
but  it  varies  according  to  the  heart  rate  and  the  degree 
of  stenosis.  If,  while  the  regular  heart  beats  are  present, 
there  are  short  presystolic  murmurs,  these  murmurs  usually 
vanish  when  fibrillation  begins  ;  and  more  especially 
if  the  rate  during  fibrillation  is  rapid.  If  the  presystolic 
murmur  is  long  and  rough,  a  murmur  of  similar  character  is 
preserved  during  fibrillation.  But  its  time  relations  are 
altered.  Attention  should  concentrate  upon  the  position  of 
the  second  sound  at  the  apex.  When  the  auricle  is  fibrillating, 
the  diastolic  murmur  has  a  fixed  time  relation  to  this  sound. 
If  the  heart  rate  is  rapid,  the  murmur  begins  early  in  diastole 
and  fills  the  whole  gap  to  the  first  sound  of  the  succeeding 
beat  (Fig.  48)  ;  if  the  heart  rate  is  less  rapid,  the  murmur 
maintains  its  relation  to  the  second  sound  but  falls  short  of 
the  succeeding  first  during  the  longest  ventricular  pauses 
(Fig.  46^)  j  ^  the  heart  rate  is  slow,  a  long,  though  varying, 
interval  separates  the  end  of  the  murmur  and  the  next  first 
sound  ;  the  murmur  is  then  confined  to  early  diastole  (Fig. 
50).  The  whole  series  of  murmur  arrangements  may  be 
observed  in  a  single  case  which  exhibits  different  heart  rates 
from  time  to  time.  The  reason  of  the  changes  will  be  clear 
when  the  pressures  and  mechanism  are  considered.  The 
diastolic  murmurs  of  mitral  stenosis  are  dependent  upon  the 
rate  of  flow  through  the  constricted  orifice,  and  the  rate  of 
flow  is  controlled  by  the  difference  of  pressure  in  auricle  and 
ventricle  at  any  given  moment.  Now  although  the  auricular 
pressure  exceeds  the  ventricular  during  the  whole  of  diastole, 
the   excess   is   greatest   at   two   phases,   namely,    when   the 


92  Chapter    VII. 

auricle  is  in  contraction  and  directly  after  the  opening  of  the 
mitral  valves.  Where  the  auricle  contracts  in  normal 
fashion,  mitral  diastolic  murmurs  are  in  chief  evidence  at 
first  in  late,  and  afterwards  in  early  diastole  ;  they  are  found 
in  early  diastole  when  the  auricle  is  virtually  paralysed, 
especially  when,  the  heart  rate  being  slow,  stasis  raises  the 
ventricular  pressure  during  the  last  phases  of  diastole. 

The  clinical  recognition  of  auricular  fibrillation  rests 
primarily  upon  the  nature  of  the  ventricular  action,  but  it  is 
aided,  as  we  have  seen,  by  certain  additional  phenomena. 
It  is  possible,  too,  to  formulate  a  few  general  rules,  which 
serve  as  useful  guides  to  its  identification.  When  the 
ventricle  beats  irregularly  at  a  rate  surpassing  120  per  minute, 
the  irregularity  is  almost  always  of  this  nature.  When 
an  irregular  ventricular  action  accompanies  signs  and 
symptoms  of  serious  heart  failure,  it  is  probably  the  result  of 
auricular  delirium,  and  the  probability  is  increased  if  the 
heart  rate  is  much  accelerated.  In  patients  in  whom  the 
heart  is  irregular,  but  in  whom  the  heart  rate  is  not  much 
accelerated  and  in  whom  signs  of  heart  failure  are  absent 
or  few,  a  test  may  be  applied  which  is  of  considerable  value. 
Moderate  exercise  augments  the  ventricular  rate,  and 
this  is  so  whether  fibrillation  is  present  or  not  ;  but  there 
is  a  striking  contrast  in  two  given  cases  of  irregularity,  of 
which  one  is  due  to  auricular  fibrillation,  while  the  other  has  a 
different  cause  (i.e.  premature  beats,  partial  heart-block, 
etc.).  In  fibrillation  the  pulse  becomes  more  irregular 
with  its  acceleration,  while  in  the  remainder  the  pulse 
steadies.  When  premature  beats  are  present,  a  sufficient 
acceleration  of  ventricular  rate  to  abolish  them  temporarily 
may  often  be  induced  by  several  quick  changes  from  the 
recumbent  to  the  sitting  posture  ;  this  is  not  so  where 
fibrillation  is  concerned.  On  the  other  hand,  as  the  pulse 
slows  subsequent  to  exercise,  reversed  relations  are  witnessed  ; 


Auricular  Fibrillation.  93 

the  irregularity  of  fibrillation  decreases,  while  other  forms  of 
irregularity  become  more  prominent.  Fever  similarly  raises 
the  ventricular  rate  and  during  the  febrile  stage  the  disorder 
of  fibrillation  persists  and  is  often  augmented  in  degree. 
Finally,  the  persistence  of  the  irregularity,  which  is  due  to 
fibrillation,  needs  emphasis.  In  most  cases  it  is  continuous 
from  the  time  of  observation  until  death.  The  other  irregu- 
larities are  present  from  time  to  time,  so  that  there  are 
intervals  of  regular  ventricular  action  each  hour  or  each  day. 

The  general  symptomatology. 

The  symptoms  complained  of  by  patients  in  whom  the 
auricles  are  in  a  state  of  fibrillation  are  very  various,  being 
dependent  mainly  upon  the  concomitant  conditions.  They  are 
the  symptoms  of  degenerate  and  failing  heart  muscle,  and 
these  do  not  require  reiteration  at  the  present  time.  The 
symptoms  which  are  now  our  special  concern  are  those  which 
appear  to  be  the  special  developments  of  fibrillation  itself. 
Patients,  who  possess  the  persistent  disorder,  often  experience 
occasional  fluttering  in  the  chest  and  neck  and  may  be 
conscious  of  irregular  heart  action.  They  are  more  prone 
to  shortness  of  breath,  exhaustion  and  other  symptoms 
of  over-taxation  of  the  heart  than  are  those  with  similar 
valve  lesions  and  a  like  degree  of  cardiac  dilatation*  ;  but  it 
is  not  always  easy  to  allot  these  superadded  symptoms  to 
precise  causes  ;  they  are  in  part  the  result  of  the  graver 
myocardial  condition  which  consorts  with  fibrillation  ;  they 
are  iii  part  due  to  the  actual  turbulence  and  embarrassment 
of  the  ventricle. f  That  the  heart  is  taxed  by  the  irregularity 
cannot  be  doubted,  but  it  cannot  be  stated  that  any  symptom, 

*  On  the  other  hand  they  seem  peculiarly  exempt  from  angina. 

f  The  heart  embarrassment  is  the  result  of  ventricular  irregularity  and 
rapid  action  ;  the  virtual  paralysis  of  the  auricle  is  without  appreciable  effect. 
on  the  general  circulation. 


94  Chapter    VII. 

such  as  cyanosis,  conspicuous  dyspnoea,  noticeable  venous 
engorgement  or  dropsy,  is  the  direct  outcome  of  fibrillation  ; 
for  cardiac  failure  and  these,  its  classical  accompaniments, 
are  found  where  there  is  no  fibrillation,  and  instances  of 
fibrillation  are  not  rare  in  which  these  symptoms  are  not 
discoverable.  In  the  production  of  the  symptoms,  there  is, 
as  has  been  stated,  an  interplay  of  two  factors,  namely,  the 
inherent  muscle  defect  and  the  extra  burden  of  disordered 
action  ;  while  the  signs  of  failure  are  proportioned  to  the 
degree  of  muscle  damage,  the  whole  of  this  symptomatic 
scale  is  raised  by  irregularity.  In  the  healthy  hearts  of 
animals  it  is  a  general  rule  that  fibrillation  of  the  auricle 
produces  a  fall  of  arterial  and  a  slight  rise  of  venous  pressure, 
but  at  the  same  time  it  is  accompanied  by  a  decrease  in  the 
heart's  dimensions,  a  usual  phenomenon  when  the  rate  is 
increased.  The  heart  accommodates  itself  to  the  new 
conditions  in  a  few  moments  ;  the  arterial  pressure  rises  and 
the  venous  pressure  falls,  so  that  they  almost  recover  their 
previous  levels  and  the  blood  flow  is  maintained  in  a  wellnigh 
perfect  fashion  for  hours.  But  if  the  heart  has  been 
damaged,  the  effect  is  both  profound  and  lasting  and  in 
place  of  decrease  of  heart  volume,  an  increase  may  occur.  So 
it  is  in  patients.  Patients  may  experience  paroxysmal 
fibrillation  at  intervals  of  a  month  or  perhaps  a  year  ;  many  of 
them  pass  through  their  attacks  with  little  or  no  sensibility  of 
them  ;  neither  can  any  sign,  other  than  irregularity,  be 
discovered  during  their  progress.  Yet  similar  crises  give 
rise  in  other  patients  to  profound  and  serious  disturbance, 
breathlessness,  pain,  cyanosis  and  further  indications  of 
increasing  dilatation  of  the  heart.  In  these,  the  severest 
cases,  the  symptoms  resemble  those  of  long  continued 
paroxysms  of  regular  tachycardia.  Between  the  mild  and 
most  extreme  reactions  is  the  intermediate.  The  variation  in 
the  reaction  is  great,  and  as  I  have  said  is  largely  attributable 


Auricular  Fibrillation.  95 

to  the  grade  of  underlying  heart  mischief.  But  there  is 
another  and  equally  important  factor  in  the  human  subject  ; 
it  is  the  rate  of  the  ventricular  action  during  the  attack. 
Just  as  the  muscle  defect  varies  in  its  degree,  so  also  does  the 
burden  imposed  upon  it ;  thus,  in  the  extreme  instances,  it  is 
found  that  little  reaction  is  shown  in  paroxysms  of  relatively 
slow  ventricular  action,  while  amongst  those  with  grave 
disturbance  the  ventricular  rate  is  usually  rapid. 

Remarks  upon  diagnosis. 

The  diagnosis,  usually  suggested  for  cases  which  exhibit 
fibrillation  of  the  auricles,  is  still  that  of  the  accompanying 
valve  lesion,  though  I  am  strongly  of  opinion  that  it  is  no 
longer  warrantable.  A  diagnosis  should  include  either  the 
outstanding  feature  of  the  pathology,  or  it  should  be  chosen 
that  it  may  become  associated  with  some  specially  beneficial 
form  of  treatment.  In  all  these  patients  chronic  affection 
of  the  myocardium  is  the  essential  lesion  ;  while  the  relations 
of  the  cardiac  disorder  to  digitalis  medication  are  so  peculiar 
that  the  named  disorder  of  the  heart  always  brings  this 
drug  to  mind. 

But  I  wish  to  refer  but  briefly  to  this  question  of  termin- 
ology under  the  present  heading  ;  and  have  chosen  it  more 
especially  to  emphasise  a  common  and  avoidable  diagnostic 
blunder,  which  comes  from  want  of  true  appreciation 
of  the  mechanism  in  these  cases.  In  discussing  the  signs 
associated  with  fibrillation,  I  have  spoken  of  the  modification 
of  diastolic  murmurs  in  mitral  disease.  A  murmur,  which 
originally  occupies  the  full  diastole  of  the  shorter  cycles,  is 
replaced,  as  the  heart  slows,  by  an  early  diastolic  murmur 
which  is  maximal  in  the  region  of  the  apex.  It  is  the  last 
murmur  which  so  frequently  misleads  the  physician  and 
suggests  to  him  an  insufficiency  of  the  aortic  valves.  It  is  said 
that  in  some  cases  of  aortic  regurgitation  the  characteristic 


96  Chapter  VII. 

bruit  is  confined  to  the  apex,  but  I  believe  this  is  far  less 
common  than  has  been  supposed,  and  that  an  erroneous 
conception  of  its  frequency  has  arisen  from  inclusion  of  many 
of  the  cases  to  which  T  now  refer.  When  mitral  stenosis  and 
auricular  fibrillation  are  present  in  the  same  patient,  and  the 
heart  rate  is  slow,  an  early  diastolic  murmur,  most  clearly 
audible  at  the  apex  but  often  spreading  beyond  it,  is  an 
expected  sign.  A  diagnosis  of  aortic  reflux  is  never  justifiable 
when  the  heart  is  grossly  irregular  and  slow,  unless 
unequivocal  signs  of  it  are  present  apart  from  such  a  murmur. 
Uncomplicated  aortic  valvular  disease  and  fibrillation  of  the 
auricles  is  a  comparatively  rare  clinical  picture.  The 
combination,  yielding  a  purely  apical  murmur,  is  so  far  an 
undescribed  condition.  Close  attention  to  the  character  and 
accurate  timing  of  the  adventitious  sound  is  often  helpful. 
The  early  diastolic  murmur  of  mitral  stenosis  is  relatively  soft 
in  quality  and  it  usually  begins  a  little  later  than  the  second 
sound.  The  absence  of  a  waterhammer  pulse  and  of  a 
murmur  at  the  aortic  cartilage  are  evident  aids  to  a  correct 
conclusion. 

The  prognosis. 

As  in  all  other  kinds  of  heart  irregularity,  the  prognosis 
is  largely  governed  by  the  remaining  symptoms  and  signs, 
and  in  any  individual  case  an  estimate  is  formed,  which 
includes  consideration  of  the  past  history,  the  presence  or 
absence  of  serious  symptoms,  the  presence  or  absence  of 
dilatation,  of  valve  lesion,  renal  disease,  etc..  But  fibrillation 
gives  an  added  significance  to  the  case.  It  is,  as  I  have  said, 
in  itself  an  evidence  of  muscular  damage,  and  of  serious 
muscle  damage.  It  loads  an  already  defective  muscle  with 
an  extra  and  appreciable  burden.  In  most  cases  it  heralds 
cardiac  failure,  temporary  or  terminal,  so  that  few  patients 
survive  its  onset  for  more  than  ten  years.     There  are  well 


Auricular  Fibrillation.  97 

authenticated  instances  in  which  it  has  persisted  for  a  longer 
period,  but  they  are  few.  The  most  valuable  intrinsic  sign 
is  the  rate  of  the  ventricular  action,  a  persistent  rate  of  120 
or  over  is  of  serious  omen,  and  according  as  the  rate  is 
maintained  above  this  count,  so  the  outlook  becomes  graver. 
Rates  of  140  and  over  are  rarely  maintained  for  many 
months,  rates  of  160  do  not  continue  for  many  weeks.  An 
extremely  important  consideration  is  the  reaction  to  treatment. 
As  we  shall  see,  a  large  number  of  cases  react  to  cardiac  drugs  ; 
in  many,  more  especially  the  rheumatic  group,  the  rate  can 
be  controlled,  can  be  reduced  and  can  be  maintained  within 
limits  which  spare  the  heart  from  excessive  taxation  of  its 
strength.  In  dealing  with  a  patient  who  has  a  given  heart 
rate,  the  prognosis,  in  so  far  as  it  is  affected  by  the  fibrillation, 
does  not  depend  so  much  upon  the  rate  of  the  heart  beat 
observed,  as  upon  the  heart  rate  which  persists  under 
treatment.  At  the  same  time,  the  prognosis  is  more  grave 
for  a  given  rate,  when  treatment  is  required,  than  when  this 
rate  is  maintained  in  the  absence  of  remedies. 

The  treatment. 

There  is  no  ailment  in  which  such  success  can  be  achieved, 
no  other  cardiac  disorder  which  may  be  so  speedily  benefited, 
as  the  well-managed  case  of  auricular  fibrillation.  In  no 
other  affection  can  the  medical  attendant  point  with  more 
thorough  confidence  to  the  effects  of  his  remedies.  As  a 
direct  result  of  active  treatment  the  moribund  may  be 
restored  and  many  years  may  be  added  to  their  lives. 
Auricular  fibrillation  is  the  condition  to  which  drugs  of  the 
digitalis  group  owe  their  well-founded  reputation. 

The  guide  to  the  physician  is  the  rate  of  the  heart  beat, 
an  index  which  rarely  fails  him.  Auricular  fibrillation  is  an 
absolute  indication  for  the  administration  of  a  member  of  the 


93  Chapter    VII. 

digitalis  group,  whenever  the  heart  rate  exceeds  100  while 
the  patient  is  at  rest.  In  a  very  large  proportion  of  the 
patients  the  drug  acts  as  a  specific,  impeding  the  passage  of 
impulses  from  auricle  to  ventricle  and  thus  reducing  the  rate. 
If  the  heart  rate  does  not  fall  as  a  result  of  rest,  and  if  it  will 
not  fall  when  digitalis  or  an  allied  drug  has  been  properly 
administered,  no  other  remedy  is  known  which  is  of  service 
in  reducing  the  heart  rate.  In  young  people,  and  especially 
those  who  have  been  affected  by  rheumatism  or  chorea,  an 
absolute  control  of  the  rate  is  almost  always  established  and 
maintained.  The  treatment  consequently  consists  of  the 
administration  of  such  doses  as  will  keep  the  heart  rate 
within  reasonable  limits. 

It  does  not  necessarily  follow  that  a  patient  who  has 
fibrillation  should  lie  up.  But  where  the  heart  rate  exceeds 
100  it  is  advisable,  and  the  patient  should  remain  in  bed  until 
his  reaction  to  digitalis,  or  a  similar  drug,  has  been  thoroughly 
investigated.  Further  treatment  in  bed  is  decided  upon 
according  to  the  general  condition,  and  according  to  the 
tolerance  and  reaction  to  digitalis.  In  treating  cases  with 
digitalis,  it  is  found  that  in  some  the  rate  is  unaffected  ; 
these  are  chiefly  patients  of  the  non-rheumatic  group.  In  most, 
a  reaction  is  speedily  obtained.  These  latter  may  be  divided 
into  three  classes  :  the  first,  those  in  whom  the  reaction  is  a 
permanent  one  ;  these  are  patients  in  whom  the  rate  remains 
slow  though  digitalis  is  omitted  :  the  second,  those  in  whom 
the  reaction  is  permanent  when  small  doses  are  subsequently 
administered :  the  third,  those  in  whom  persistent  high 
dosage  is  required  to  maintain  control. 

As  a  routine,  the  tincture  or  fresh  infusion  of  digitalis 
is  given,  for  it  is  the  safest  and  most  potent  remedy.  The 
tincture  is  given  to  adults  in  doses  of  from  10  to  15  minims 
three  or  four  times  a  day  (the  infusion  in  1  to  1£  drachm 
doses) ;  if  the  reaction  does  not  begin  within  four  or  five  days, 


Auricular  Fibrillation.  99 

the  dosage  may  be  increased  until  symptoms  of  nausea, 
diarrhoea,  headache  or  retardation  of  the  pulse  appear.  It 
not  infrequently  happens  that  the  desired  fall  of  heart  rate 
first  comes  when  other  signs  of  intoxication  are  manifested  ; 
if  these  persist  for  several  days  the  drug  must  be  reduced  or 
omitted,  whether  the  rate  has  fallen  or  not.  The  dosage  is 
also  reduced  if  the  heart  rate  falls,  and  the  reduction  is 
continued  so  long  as  the  heart  rate  remains  below  90.  It 
may  be  diminished  to  nothing  in  many  cases  ;  often  5  minim 
doses  are  eventually  found  to  suffice.  Usually  the  full 
reaction  is  obtained  after  six  or  eight  drachms  of  the  tincture 
or  an  equivalent  quantity  of  infusion  has  been  given.  When- 
ever the  rate  has  reached  60  or  80  per  minute,  the  drug  is 
stopped,  and  it  is  given  again  only  if  the  heart  rate  begins  to 
accelerate  once  more.  The  appearance  of  coupled  heart 
beats  (Fig.  50)  is  always  a  sign  of  danger  ;  whenever  they 
appear  the  digitalis  must  be  discarded.  I  have  seen  more 
than  one  case  of  unexpected  death,  attributable  to  excessive 
dosage  with  digitalis,  at  this  stage  ;  it  must  be  remembered 
always  that  digitalis  is  a  poison,  and  that  it  has  other  actions 
than  the  simple  reduction  of  heart  rate. 

In  most  instances  where  the  patient  has  reacted,  the 
drug  can  be  stopped  without  the  recurrence  of  accelerated 
rate  so  long  as  he  remains  in  bed.  When  he  rises  from  bed 
a  renewal  of  the  small  dose  (5  minims)  may  be  necessary. 
In  other  cases  the  result  is  less  satisfactory  and  heavier  dosage 
must  continue. 

It  sometimes  happens  that  a  patient  is  peculiarly 
intolerant  to  digitalis,  and  that,  where  a  reaction  is  expected, 
a  dosage  of  1 5  to  20  minims  of  the  tincture  cannot  be  reached 
or  maintained  sufficiently  long,  without  nausea,  or  other 
discomforting  symptoms  supervening.  Strophanthus  or 
squills  may  be  tried,  starting  with  doses  of  10  minims  of  the 
tinctures.     These  drugs  are  pushed  in  the  same  manner,  but 

H  2 


100  Chapter    VII. 

though  they  are  less  apt  to  induce  nausea  or  vomiting,  and 
while  diarrhoea  is  the  chief  intestinal  disturbance  produced 
by  them,  they  are  less  reliable  than  digitalis.  In  some  of 
these  cases,  too,  recourse  may  be  had  to  intravenous  injections 
of  strophanthin. 

When  a  patient  who  has  fibrillation  is  first  seen,  and  the 
heart  beats  persistently  at  170-200  per  minute,  the  condition 
is  urgent  and  heavy  doses  of  digitalis  (minims  20  to  30)  should 
be  employed.  The  intravenous  injection  of  strophanthin 
is  also  valuable  at  such  times.  Two  or  three  doses  of  1/250 
of  a  grain,  each  in  40-60  minims  of  saline,  are  given  at  intervals 
of  two  hours.  The  reduction  of  rate  is  almost  immediate, 
and  heart  rates  of  ninety  or  eighty  are  reached  in  from  6-12 
hours.  The  remedy  should  be  employed  cautiously  and 
its  adoption  must  be  confined  to  the  urgent  case  which  belongs 
to  the  rheumatic  group  or  to  similar  cases  in  which  medication 
by  the  mouth  has  been  hindered  by  the  onset  of  gastro- 
intestinal symptoms. 

A  relatively  small  group  of  cases  of  auricular  fibrillation 
remains  where,  with  persistently  high  ventricular  rate,  digitalis 
has  little  or  no  influence  ;  these  patients  are  also  unaffected 
by  strophanthus  and  squills.  In  so  far  as  the  fibrillation  and 
excessive  heart  rate  are  concerned,  nothing  further  can  be 
done  for  them. 

The  treatment  of  the  case  of  auricular  fibrillation,  in  the 
patient  who  is  up  and  about,  is  guided  mainly  by  the  rate  of 
the  heart  and  the  urgency  of  the  patient's  symptoms.  The 
disorder  is  generally  persistent,  and  most  hospital  patients 
eventually  leave  their  beds  and  return  to  their  former 
occupations.  But  even  where  the  pulse  rate  is  persistently 
low  and  symptoms  are  few,  excessive  exertion  should  be 
avoided  ;  heavy  manual  labour,  strenuous  games  or  sports 
should  form  no  further  part  in  the  daily  life.  If  the  pulse  rate 
quickens  readily,  if  drugs  are  constantly  required  to  maintain 


Auricular  Fibrillation.  101 

the  retardation,  and  especially  if  breathlessness  or  precordial 
uneasiness  are  easily  induced,  further  restrictions  are 
necessary.  All  patients  of  the  female  sex  should  be  specially 
warned  of  the  strain  and  danger  of  pregnancy. 

Regular  meals  consisting  only  of  a  sufficiency  of  solid 
and  sustaining  food,  preferably  dry  ;  early  hours  ;  a  placid 
existence  ;  the  avoidance  of  public  buildings  and  all  places 
and  seasons  in  which  influenza  and  bronchitic  troubles  are 
contracted  ;  and,  lastly,  scrupulous  attention  to  the  hygiene 
of  the  teeth  and  throat,  are  sound  directions  in  this  as  in 
other  serious  heart  maladies. 

Belladonna,  its  ally  hyoscyamus  and  their  extractives 
should  be  avoided.  Their  customary  action  is  to  increase  the 
rate  of  the  ventricle  considerably  in  this  condition. 

In  cases  of  urgency,  or  where  the  patient's  life  may  be 
considerably  prolonged  by  surgical  operation,  general  anaes- 
thetics may  be  employed.  But  where  there  is  any  hesitancy 
to  perform  an  operation,  apart  from  the  cardiac  condition, 
the  presence  of  fibrillation  should  countermand  it. 

Paroxysmal  fibrillation. 

Most  hearts  which  develop  fibrillation  of  the  auricles 
maintain  this  mechanism  to  the  end  of  the  chapter  ;  it  is 
essentially  a  chronic  and  terminal  malady.  But  from  time  to 
time  transient  attacks  are  seen,  and  in  some  patients 
paroxysms  of  fibrillation  of  a  few  hours,  days  or  weeks 
duration  are  noted.  The  affection,  when  it  takes  this  form, 
is  generally  classed  as  paroxysmal  tachycardia.  In  my 
discussion  of  paroxysmal  tachycardia  I  have  excluded  it, 
desiring  to  deal,  as  I  did,  with  the  simpler  mechanism  alone. 

The  exact  frequency  of  the  paroxysmal  affection  has  not 
been  ascertained,  but  it  may  be  gauged  approximately  by 
comparison.  Of  the  152  cases  of  auricular  fibrillation 
included  in  the  table  on  page  86,  in  only  16  was  the  disorder 


102  Chapter  VII. 

temporary  and  recurring.  Paroxysms  of  regular  tachycardia 
appear  to  be  more  common  ;  as  opposed  to  the  16  irregular 
tachycardias,  simple  and  regular  paroxysms  have  been  seen 
in  45  patients. 

The  symptoms  of  paroxysmal  fibrillation  have  been 
spoken  of  already.  They  may  be  inconspicuous  or  profound. 
When  the  rate  of  ventricular  response  is  rapid  (160-200 
per  minute)  the  symptoms  are  those  of  simple  tachycardias 
at  similar  rates,  though  they  are  on  the  whole  more  severe. 
The  prognosis  is  reasoned  in  the  manner  stated  for  regular 
paroxysms  ;  the  management  and  symptomatic  treatment  of 
the  attacks  are  similar  in  the  two.  A  few  words  are  necessary 
upon  digitalis  medication.  Drugs  belonging  to  this  group 
have  been  known,  not  infrequently,  to  excite  fibrillation  in 
those  predisposed.  They  are  therefore  contra-indicated  in 
paroxysms  of  short  duration  and  in  those  which  produce  few 
symptoms.  Where  the  paroxysms  are  more  prolonged,  or 
where  the  symptoms  are  urgent,  they  may  be  given  to 
advantage  ;  and,  if  given,  dosage  should  be  arranged  for  a 
speedy  reaction.  In  such  patients,  the  reaction  consists  of 
slowing  of  the  ventricular  rate  and  is  therefore  beneficial, 
but  the  duration  of  the  paroxysm  is  usually  prolonged  by 
the  administration. 


(     103     ) 


Chapter  VIII. 


ALTERNATION    OF    THE    PULSE. 

Definition. 
A  condition  in  which  the  left  ventricle,  while  beating 
regularly,    expels    larger    and    smaller    quantities    of    blood 
at    alternate    contractions. 

The  mechanism  in  alternation  of  the  pulse. 

Alternation  in   the   size   of  pulse   beats,   so    that  each 

alternate  beat  is  large  and  each  alternate  beat  is  small  is  of 

obscure  origin.     The  contractions  of  the  ventricle  are  regular, 

and  each  is  preceded  at  a  normal  interval  by  a  contraction  of 


A 


I  I  I  I  I 

\_  x'    \_  v_ 

urn 


Fig.  51.  A  diagrammatic  representation  of  alternation  of  the  heart.  The 
auricular  and  ventricular  beats  are  placed  regularly  and  in  order,  but 
alternate  ventricular  contractions  are  weak. 

the  auricle  (Fig.  51).  The  disturbance  is  dependent  upon 
some  unexplained  anomaly  of  the  ventricular  systoles, 
whereby  at  each  alternate  systole  of  the  left  ventricle  a 
greater  or  lesser  quantity  of  blood  is  thrown  into  the  systemic 


104  Chapter    VIII. 

arteries.     In  the  figure,  I  have  represented  this  anomaly  by 
varying  the  size  of  the  ventricular  rectangles. 

Etiological  and  pathological  relations. 

Alternation  of  the  pulse  is  seen  in  two  classes  of  patient. 

First,  it  occurs  in  those  in  whom  the  heart  rate  is  unduly 
accelerated  and  more  especially  as  an  accompaniment  of 
paroxysmal  tachycardia.  Associated  with  paroxysmal 
tachycardia,  it  has  etiological  and  pathological  relations  in 
common  with  the  last  named  disorder  ;  its  prognostic  signifi- 
cance is  not  fully  known,  but  as  it  depends  chiefly,  if  not 
entirely,  upon  acceleration  of  the  heart  rate,  it  may  be 
regarded  almost  as  a  physiological  reaction  to  the  increased 
frequency  of  beat. 

Secondly,  it  occurs  when  the  heart  rate  lies  within 
normal  limits  and  at  such  times  it  is  a  sign  of  much  clinical 
value.  Seen  in  elderly  subjects  and  pre-eminently  in  the 
male  sex,  it  consorts  especially  with  angina  pectoris,  high 
arterial  pressure,  renal  disease,  and  fibrotic  myocarditis. 
It  has  been  seen  in  pneumonia  during  the  pre-critical  stage, 
and  also  in  patients  under  the  influence  of  large  doses  of 
digitalis. 

It  is  encountered  in  experiment  under  similar  circum- 
stances, namely,  when  the  heart  rate  is  extremely  rapid,  or 
when  it  has  been  injured  by  the  intravascular  injection  of 
poisons. 

Whenever  it  occurs,  there  is  reason  to  believe  either  that 
a  tolerably  healthy  heart  muscle  is  carrying  an  excessive 
burden,  or  that  a  diseased  or  poisoned  muscle  is  struggling 
to  perform  work  of  which  it  is  barely  capable. 

In  the  remainder  of  this  chapter,  I  shall  allude  to  pulse 
alternation  as  an  accompaniment  of  heart  rates  which  are 
not  high.  When  the  heart  is  disposed  to  alternate,  the 
actual  alternation  is  unmasked  by  anything  which  imposes  a 


Alternation  of  the  Pulse.  105 

fresh  and  added  strain  upon  that  organ.  Thus  it  is  often 
made  manifest  by  a  slight  acceleration  of  pulse  rate  ;  and, 
in  the  earlier  stages  of  its  development,  it  is  frequently 
brought  to  light  by  the  occurrence  of  a  single  premature  beat  ; 
under  the  last  named  circumstance  it  follows  immediately 
upon  the  disturbance,  and  continues  for  a  varying  number 
of  heart  cycles. 

The  recognition  of  pulsus  alternans. 

It  is  an  unfortunate  fact,  but  nevertheless  true,  that 
most  instances  of  pulsus  alternans  cannot  be  recognised  by 
other  than  instrumental  means.    There  are  patients  in  whom 


Fig.  52.     Alternation  of  the  pulse.     Each  alternate  beat  is  strong  and  each 
alternate  beat  is  weak. 


(Ui-l 


II  II  II 


Aft*- 

i/V 


Fig  53.  Apex  and  radial  curves  and  heart  sounds  in  heart  alternation, 
The  curve  is  taken  at  a  faster  rate  than  the  last  and  shows  the  slight 
variation  in  pulse  pauses.  As  opposed  to  the  picture  when  premature 
beats  are  present,  the  stronger  beat  is  followed  by  the  longer  pause. 

it  affects  the  pulse  continuously,  and  in  whom  alteration  in 
the  force  of  alternate  pulse  beats  is  perceptible  to  the  finger*  ; 
but  such  cases  are  rare,  and  identification  of  the  condition 
from  the  feel  of  the  pulse  is  most  uncertain.  Examination  of  the 

*  The  separation  from  a  dicrotic  pulse  is  easy  ;    for  where  the  latter  is 
present  the  beating  of  the  pulse  is  at  twice  the  rate  of  the  ventricle. 


106  Chapter    VIII. 

apex  beat  gives  little  assistance, for  the  heart  beats  with  regular 
rhythm  and  the  differences  in  the  force  of  ventricular  systoles 
and  the  intensity  of  the  heart  sounds  are  inappreciable. 

It  is  a  sign  of  such  importance  and  is  so  readily 
overlooked,  that  it  should  be  sought  deliberately  whenever 
there  is  reason  to  suspect  the  possibility  of  its  presence. 
Thus  it  is  wise  to  examine  all  cases  of  angina  pectoris, 
all  cases  of  high  blood  pressure  and  all  elderly  subjects 
in  whom  affection  of  the  heart  is  suspected,  or  renal  disease 
is  known  to  exist,  with  a  specific  object,  namely,  to  determine 
its  presence  or  absence.  It  should  be  looked  for,  too, 
in  all  elderly  people  in  whom  premature  beats  are  frequent. 
If  such  methods  are  adopted  it  will  not  often  escape  detection. 
It  is  so  frequently  confined  to  the  few  cycles  which  follow  a 
premature  beat  that,  in  any  one  of  the  classes  of  patient 
mentioned,  it  is  most  useful  to  obtain  a  curve  which  contains 
such  a  beat.  This  may  often  happen  at  the  first  examination. 
The  patient  should  remain  standing,  for  premature  beats  are 
more  frequent  in  this  posture,  and  if  he  has  come  some  distance r 
it  is  well  that  the  examination  should  proceed  at  once,  since 
premature  beats  are  more  conspicuous  at  such  times.  It 
should  be  remembered  too,  that  a  held  breath  may  evoke 
a  premature  beat  and  the  opportunity  of  catching  it  in  this 
manner  should  not  be  lost. 


»  »   y«'y^vT'«r»v»»y»<r»y»»»   * 


Fig.  54.     Alternation  of  the  pulse,  appearing  after,  and  as  a  result  of,  a 
single  premature  beat  p.     It  lasts  for  four  heart  cycles. 

Single  premature  beats  are  usually  followed  by  a  pulsa- 
tion of  exceptional  size,  for  the  heart  puts  out  more  than  its 
usual  quantum  of  blood.  It  is  the  pulse  which  succeeds  this 
tall  beat  which  shows  the  first  sign  of  alternation  ;   it  is  less 


Alternation  of  the  Pulse.  107 

forcible  than  that  which  succeeds  it.  In  Fig.  54  a  regular 
pulse  is  interrupted  by  a  single  premature  contraction  (p)  ; 
it  is  followed  by  the  usual  pause  and  this  is  succeeded  by  a  tall 
pulsation  (I)  ;  the  next  beat  s1  is  small,  it  is  followed  by  a 
taller  beat  I1.  The  small  beat  s1  is,  as  I  have  said,  the  earliest 
sign  of  the  condition,  and  it  may  be  the  sole  sign.  In  the 
actual  figure  s2,  the  alternate  beat,  is  also  low.  Alternation 
has  proceeded  for  four  cycles  before  the  normal  pulse  beats 
are  restored.  In  Fig.  52  and  53  the  condition  is  persistent 
throughout  each  curve  ;  little  and  big  beats  are  arranged 
alternately.  Extreme  degrees  of  alternation  of  the  pulse 
are  seldom  encountered  ;  but  on  very  rare  occasions  the 
little  beats  vanish  entirely,  and  the  pulse  rate  is  halved. 

The  other  irregularity  with  which  pulsus  alternans  may 
be  confused  is  a  coupled  pulse  resulting  from  premature 
beats,  but  this  only  happens  where  the  prematurity  of  the 
second  beat  of  each  couple  is  slight.  An  example  is  shown 
in  Fig.  33  of  an  earlier  chapter.  There  is  a  sufficient  contrast 
between  them  ;  whereas  the  little  beat  in  Fig.  33  is  followed 
by  the  longer  pause,  if  pulsus  alternans  is  present  the  little 
beat  is  followed,  if  there  is  any  variation  in  pauses,  by  a 
slightly  shorter  pause.  In  tracings  written  upon  slowly 
travelling  paper  the  difference  in  intervals  is  hardly  perceptible 
(Fig.  52)  ;  but  where  the  paper  has  moved  faster,  a  measure- 
able  difference  is  often  found  ;  it  is  well  seen  in  Fig.  54,  in 
which  the  pauses  following  I  and  I1  are  longer  than  those 
following  s1  and  s2. 

The  subjective  sensations  of  patients  presenting   pulsus 

alternans. 
Alternation  of  the  heart  is  itself  responsible  for  no 
symptoms  ;  the  patient  only  complains  of  sensations  which 
are  referable  to  other  causes.  Thus,  anginal  pain  is  common. 
Breathlessness  is  even  commoner  ;  it  is  often  nocturnal, 
repeatedly  awakening  the  subject  of  it  after  short  periods 


108  Chapter    VIII. 

of  sleep  and  being  accompanied  by  acute  anxiety.  Breathing 
of  the  Cheyne-Stokes  type  is  rarely  noted  by  those  who 
manifest  this  respiratory  abnormality,  but  periodic  dyspnoea 
may  be  remarked  by  the  friends,  especially  by  those  who 
sleep  with  the  patients. 

The  prognosis. 

Alternation  of  the  pulse  belongs  to  a  small  group  of 
phenomena  witnessed  by  those  who  attend  the  sick,  which, 
treated  as  isolated  signals,  are  in  themselves  emphatic  and 
portentious.  It  ranks  with  subsultus  tendinum,  with  optic 
neuritis,  with  the  risus  sardonicus  and  other  ill-omened 
messengers.  It  is  the  faint  cry  of  an  anguished  and  fast 
failing  muscle,  which,  when  it  comes,  all  should  strain  to  hear, 
for  it  is  not  long  repeated.  A  few  months,  a  few  years  at 
most,  and  the  end  comes. 

How  grave  is  the  condition  of  the  patient  whose  heart 
produces  this  alternating  pulse  is  often  witnessed  to  by 
associated  signs  ;  angina,  nocturnal  dyspnoea,  Cheyne-Stokes 
breathing  or  high  blood  pressure  are  often  encountered  in  the 
same  subject.  But  here  lies  its  special  significance  :  each 
and  everyone  of  these  signs  may  fail,  and  alternation  may 
appear  alone  to  foretell  the  future.  Unexpected  death  is  a 
common  termination. 

I  write  of  continued  alternation,  of  the  pulse  which 
alternates  in  force  for  many  cycles.  It  is  persistent  while 
the  heart  yet  lives.  The  prognostic  value  of  the  lesser  grades 
of  perverted  mechanism  is  less  certainly  known  ;  but  that 
their  significance  is  grave,  and  that  they  are  but  too  often 
the  forerunners  of  the  fully  developed  condition,  should  be 
understood.  A  favourable  prognosis  is  always  forbidden  by 
the  latter,  and  can  be  but  rarely  justified  in  the  presence  of  the 
former.  The  only  propitious  circumstances  are  a  history  of 
exceptional  and  prolonged  strain  in  the  patient  who  shows  the 


Alternation  of  the  Pulse.  109 

sign,  strain  which  may  be  at  once  and  permanently  avoided, 
and  evidences  of  acute  intoxication  which  is  vanishing. 

The  treatment. 

The  management  of  heart  cases,  in  so  far  as  it  is  affected 
by  the  presence  of  alternation,  may  be  stated  in  a  few  words, 
for  it  should  be  evident.  Alternation  is  a  sign  of  overtaxation  ; 
it  demands  relief.  In  the  busy  it  calls  for  prompt  and 
drastic  curtailment  of  the  work,  be  it  mental  or  physical 
exertion.  In  the  more  sedentary,  it  is  an  indication  for 
prolongation  of  the  hours  of  actual  rest,  both  of  body  and 
mind  ;  the  condition  of  such  patients  may  undergo  temporary 
relief  by  a  long  period  of  absolute  quiescence.  In  each  case 
the  avoidance  of  all  sources  of  anxiety  or  emotion  is  to  be 
enjoined.  The  presence  of  alternation  forbids  the  adminis- 
tration of  general  anaesthetics  in  major  operations,  unless 
the  withholdment  of  the  first  immediately  jeopardises 
life,  or  unless  one  or  other  is  necessitated  for  the  relief  of 
intolerable  pain. 


(    no    ) 


INDEX 


Accentuated  first  sound 

28 

Page 

&  49 

Adams-Stokes'  Syndrome 

33 

Alternation  of  the  pulse 

103 

Angina  and 

104 

Associated  conditions 

104 

Definition  of 

103 

Etiology  of 

104 

Example  of 

3 

Heart  rate  and 

104 

In  experiment 

104 

Mechanism  of 

103 

Prognostic  value  of 

108 

Recognition  of 

105 

Subjective  sensations 

107 

Treatment  of 

109 

Anesthetics  and  disordered  heart  action 

70,   101 

&  109 

Angina 

Alternation  and 

104 

Auricular  fibrillation  and 

93  (footnote) 

Paroxysmal  tachycardia  and 

63 

As-Vs    interval 

17 

Prolongation  of 

17 

&  24 

Auricular  fibrillation 

82 

Associated  conditions 

85 

Auricular  flutter  and 

81 

Definition  of 

82 

Digitalis  and 

98 

Example  of 

3 

Heart-block  and 

84 

&  98 

Heart  rate  and 

5,  81,  92 

&  98 

Heart  sounds  in    .  . 

..   90,  91 

&  95 

Mitral  stenosis  and 

91 

Morbid  anatomy  in 

87 

Index. 


Ill 


Auricular  fibrillation,  continued — 
Nature  of   .  . 
Paroxysmal 
Prognosis  in 
Recognition  of 
Relation  to  age 
Relation  to  infective  disease 
Relation  to  sex 
Remarks  upon  diagnosis 
Rheumatic  fever  and 
Strophanthin  and 
Symptomatology  of 
Treatment  of 

Auricular  flutter 

Associated  conditions 
Auricular  fibrillation  and 
Definition  of 
Digitalis  and 
Example  of 
Heart-block  and 
Morbid  anatomy  in 
Nature  of   .  . 
Prognosis  in 
Recognition  of 
Relation  to  age,  etc. 
Strophanthin  and 
Symptomatology  of 
Treatment  of 

Auricular  sounds 

Auricular  waves 
In  arteries 
In  veins 

auriculo-ventricular  node  and  bundle 

Common  types  of  disorder 
Coupled  beats 
Gross  irregularity  of  pulse 
Halved  pulse  rate 
Mild  irregularity  of  pulse 
Solitary  pulse  intermittences 
Triple  beating 


6,   2' 


Page 

82 

101 

96 

87 

84 

85 

84 

95 

85 

100 

93 

97 

71 

74 

81 

71 

81 

3 

72 

74 

71 

74 

74 

74 

SI 

77 

81 

24  &  29 

29 

29  &  49 

16  &  23 

5 

47,  77  &  99 

7  &  82 

6,  27  &  47 

7  &  82 

26,  45  &  47 

6  &  47 

112 


Index. 


Compensatory  pause 
Coupled  beats 


Page 
41 

6,  27,  47  &  99 

Digitalis 

Auricular  fibrillation  and           .  .          .  .          .  .          . .          .  .  97 

Auricular  flutter  and        .  .           .  .           .  .           . .           .  .           .  .  81 

Heart-block  and 23,  37  &  98 

Paroxysmal  tachycardia  and.       .  .          .  .          .  .          .  .          .  .  70 

Premature  beats  and         .  .          . .          .  .          .  .          .  .          44  &   54 

Sinus  irregularity  induced  by                  .  .          .  .          .  .          .  .  14 

Diastolic  murmurs  (see  Presystolic  murmur  and)  25,  28,  49,  91  &  95 

Diphtheria  and  heart-block     .  .          . .          . .          . .          . .          . .  21 

Disordered  action  of  the  heart 

Age  incidence        .  .          .  .          .  .          .  .          .  .          .  .          .  .  4 


Frequency 
Heart  rate  and 
Persistence 

Dropped  beats 

Gross  irregularity 

Halved  heart  rate  (see  Heart  rate 

Halved  pulse  rate 

Heart-block 

Blood  pressure  in 

Complete 

Definition  of 

Digitalis  and 

Diphtheria  and 

Effect  of  {on  the  circulation) 

Etiology 

Example  of 

Fits  in 

Grades  of    .  . 

Heart  rate  in 

Heart  sounds  in 

Heredity  and 

Hypertrophy  in 

Influenza  and 

Mitral  stenosis  and 


4 
4 
5 

17  &  25 


•   6, 

27  &  47 

16 

32 

20  &  29 

16 

.  23, 

37  &  98 

21 

31 

20 

2 

33,  35, 

36  &  38 

17-20 

&  24-31 

4,  26, 

29  &  33 

•  24, 

28  &  29 
21 
32 
21 

25  &  28 

Index. 


113 


Heart-block  {continued) 

PAGE 

Morbid  anatomy  in 

23 

Nature  of 

16 

Pneumonia  and 

21 

Prognosis  in 

34 

Recognition  of 

24 

Relation  to  age 

20 

Relation  to  chronic  degeneration 

22 

Relation  to  infective  disease- 

21 

Relation  to  sex 

20 

Rheumatic  fever  and 

21 

&  22 

Symptoms  of 

31 

Syphilis  and 

21-23 

Treatment  of 

36 

2  :  1  heart  block 

19 

&  26 

Typhoid  and 

21 

Vagus  and 

23 

Heart  rate 

Alternation  and 

93 

Auricular  fibrillation  and 

5,  84, 

92 

&  98 

Auricular  flutter  and 

71-73 

Fast             

..4  &  57 

Halved 

..7  &  26 

Heart-block  and 

4,  26, 

29 

&  33 

Premature  contractions  and 

5 

&  44 

Sinus  irregularity  and 

5 

&   15 

Slow              

..   4,   10,  26, 

29 

&  84 

Heart  sounds 

Auricular  fibrillation  and 

..90, 

91 

&  95 

Auricular  sounds 

24 

&  29 

First  sound  intensified 

29 

&  49 

First  sound  reduplicated 

25 

Grouping  of 

45 

Heart-block  and 

.  .          .  .    24, 

28 

&  29 

Mitral  stenosis  and 

25,  28,  60, 

91 

&  95 

Paroxysmal  tachycardia  and 

60 

Premature  contractions  and 

45 

&  47 

Second  sound  reduplicated 

25 

Influenza 

Auricular  fibrillation  and 

86 

Auricular  flutter  and 

74 

Heart-block  in 

<    .                     .    . 

21 

114 


Index. 


Intermittence  of  pulse 

Mitral  stenosis 

Auricular  fibrillation  and 
Heart-block  and 
Heart  sounds  in    .  . 
Paroxysmal  tachycardia  and 

Morbid  anatomy 

Auricular  fibrillation  and  its 
Auricular  flutter  and  its 
Heart-block  and  its 
Paroxysmal  tachycardia  and  its.  . 

Pacemaker 

Paroxysmal  tachycardia  (simple  form 
Angina  and 
Associated  conditions 
Definition  of 
Differential  diagnosis  of 
Factors  promoting  attacks 
Heredity  and 
Mitral  slen 
Morbid  ana 
Nature  of 
Posture  and 
Premature  contr 
Prognosis  o. 
Relation  to 

Relation  to  infective  diseases 
Relation  to  sex 
Rheumatic  fever  and 
Symptomatology  of 
Syphilis  and 
Treatment  of 

Phasic  variations  of  pulse  rate 


Page 

5, 

45 

& 

47 
74 

25 

& 

28 

25, 

28, 

60, 

91 

& 

95 

58 

& 

60 

87 
74 
23 
59 

Pneumonia 

Alternation  and 
Heart-block  and 


104 
21 


Index. 


115 


Pre  mature  contractions 

Associated  conditions 

Auricular 

Definition  of 

Digitalis  and 

Example  of 

Fatigue  and 

Heart  rate  and 

Heart  sounds  in    .  . 

Nature  of    .  . 

Paroxysmal  tachycardia  and 

Posture  and 

Prognosis  of 

Provocative  factors 

Recognition  of 

Relation  to  age 

Relation  to  sex 

Subjective  phenomena  in 

Tobacco  and 

Treatment  of 

Ventricular 

Presystolic  murmur  (disappearance  or) 

Prognosis 

Alternation  of  the  heart  and 
Auricular  fibrillation  and 
Auricular  flutter  and 
Heart-block  and 
Paroxysmal  tachycardia  and 
Premature  contractions  and 
Sinus  irregularity  and 

Pulsus  alternans  (see  alternation  of  the  pulse) 

Pulse  rate  (see  Heart  rate) 
Halved  pulse  rate 

purkinje  network 

Reduplicated  first  sound 

,,  SECOND   sound 

Refractory  state 
Respiratory  irregularities 


Page 

39 

43 

41  &  47 

39 

44  &  54 

2 

44 

5  &  44 

45  &  47 

39 

p 

>6  &  GO 

45 

52 

44 

45 

42 

43 

51 

44 

54 

40  &  47 

49,  60  &  91 

103 

96 

80 

34 

66 

52 

15 

103 

6,  2 

3  &  47 

16 

25 

25 

41 

11 

116 


Index. 


Rheumatic  fever 

Auricular  fibrillation  and 
Auricular  flutter  and 
Heart-block  and 
Paroxysmal  tachycardia  and 

slno -auricular  node 
Sinus  irregularities 

Definition  of 

Digitalis  and 

Example  of 

Heart  rate  and 

Nature  of   .  . 

Phasic  variation 

Prognostic  significance  of 

Recognition  of 

Relation  to  respiration 

Standstill  of  the  heart 

Tuberculosis  meningitis  and 
Slow  pulse 

Standstill  of  the  heart 
Strophanthin  and  auricular  fibrillation 
Sympathetic  nerves 
Syphilis 

Auricular  flutter  and 

Heart-block  and 

Paroxysmal  tachycardia  and 

Tobacco  and  pulse  irregularity 
Treatment 

Alternation  of  the  pulse  and 

Auricular  fibrillation  and 

Auricular  flutter  and 

Heart-block  and 

Paroxysmal  tachycardia  and 

Premature  contractions  and 
Triple  beating 
Tuberculous  meningitis  and  irregular  pulse 
Typhoid  and  heart-block 

Vagus 

Venous  pulsation 


Page 
85 
74 
21  &  22 


8 

14 

2 

.5  &  15 

8 

14 

15 

14 

11  &   14 

It 

15  (footnote) 
10,  26,  29,  47  &  84 
14 
100 


74 
21-23 

58 

44 

109 

97 
81 
36 
68 
54 
6  &  47 
15  (footnote) 
21 

10,  23  &  75 

29,  49  &  77 


SHAW  &  SONS,  FETTER  LANE,  LONDON,  EX. 


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